Name | complex I |
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Synonyms | 39kD; CI 39kD; Complex I; Complex I 39kD; NADH dehydrogenase (ubiquinone) Fe S protein 2 like; NADH ubiquinone oxidoreductase 39 kDa subunit mitochondrial; NADH ubiquinone oxidoreductase 39 kDa subunit; NDUFA 9… |
Name | rotenone |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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15890011 | Zeevalk GD, Bernard LP: Energy status, ubiquitin proteasomal function, and oxidative stress during chronic and acute complex I inhibition with rotenone in mesencephalic cultures. Free Radic Biol Med. 1997;22(3):439-46. |
112(1,2,2,2) | Details |
16464752 | Zhang X, Rojas JC, Gonzalez-Lima F: Methylene blue prevents neurodegeneration caused by rotenone in the retina. Eur J Cancer. 1997 Mar;33(3):421-4. Rotenone is a widely used pesticide that inhibits complex I, the first enzyme of the mitochondrial respiratory chain. |
88(1,1,2,3) | Details |
17241123 | Sherer TB, Richardson JR, Testa CM, Seo BB, Panov AV, Yagi T, Matsuno-Yagi A, Miller GW, Greenamyre JT: Mechanism of toxicity of pesticides acting at complex I: relevance to environmental etiologies of Parkinson's disease. J Biol Chem. 2005 May 20;280(20):19911-24. Epub 2005 Mar 11. The pesticide rotenone (ROT) inhibits complex I and reproduces features of PD in animal models, suggesting that environmental agents that inhibit complex I may contribute to PD. |
87(1,1,1,7) | Details |
18685029 | Costa C, Belcastro V, Tozzi A, Di Filippo M, Tantucci M, Siliquini S, Autuori A, Picconi B, Spillantini MG, Fedele E, Pittaluga A, Raiteri M, Calabresi P: Electrophysiology and pharmacology of striatal neuronal dysfunction induced by mitochondrial complex I inhibition. J Neurosci. 2008 Aug 6;28(32):8040-52. The pesticide rotenone inhibits mitochondrial complex I and reproduces features of these basal ganglia neurological disorders in animal models. |
83(1,1,1,3) | Details |
16864419 | Zhang X, Jones D, Gonzalez-Lima F: Neurodegeneration produced by rotenone in the mouse retina: a potential model to investigate environmental pesticide contributions to neurodegenerative diseases. Ann N Y Acad Sci. 2003 Jun;991:111-9. Rotenone is a widely used pesticide and fish toxin that inhibits complex I of the mitochondrial respiratory chain. |
83(1,1,1,3) | Details |
14727190 | Gonzalez-Halphen D, Maslov DA: NADH-ubiquinone oxidoreductase activity in the kinetoplasts of the plant trypanosomatid Phytomonas serpens. Biokhimiia. 1989 Sep;54(9):1571-5. Rotenone at 2-10 microM inhibited the activity 50-75%, indicating that it belongs to respiratory complex I. |
83(1,1,1,3) | Details |
12702446 | Veiga A, Arrabaca JD, Sansonetty F, Ludovico P, Corte-Real M, Loureiro-Dias MC: Energy conversion coupled to -resistant respiration in the yeasts Pichia membranifaciens and Debaryomyces hansenii. Mol Pharmacol. 1995 Nov;48(5):928-37. In both yeasts the presence of complex I was confirmed by the inhibition of consumption in isolated mitochondria by rotenone. |
82(1,1,1,2) | Details |
19767442 | Drechsel DA, Patel M: Differential contribution of the mitochondrial respiratory chain complexes to reactive species production by redox cycling agents implicated in parkinsonism. Proc Natl Acad Sci U S A. 1970 Mar;65(3):763-70. Interestingly, at micromolar (< or = 300 microM) concentrations, PQ-induced H2O2 production was unaffected by complex I inhibition via rotenone, whereas DQ-induced H2O2 production was equally attenuated by inhibition of complex I or III. |
82(1,1,1,2) | Details |
14529466 | Kotake Y, Ohta S: MPP+ analogs acting on mitochondria and inducing neuro-degeneration. Biochim Biophys Acta. 2004 Oct 4;1658(3):212-24. Spectroscopic analyses and structure-activity relationship studies have indicated that the V-shaped structure of the rotenone molecule is critical for binding to the rotenone binding site on complex I. |
87(1,1,1,7) | Details |
19158951 | Fink BD, O'Malley Y, Dake BL, Ross NC, Prisinzano TE, Sivitz WI: Mitochondrial targeted and fuel selectivity in endothelial cells. Free Radic Biol Med. 2007 Mar 1;42(5):642-53. Epub 2006 Dec 14. In mitochondria respiring on differing concentrations of complex I substrates, mitoquinone and rotenone had interactive effects on ROS consistent with redox cycling at multiple sites within complex I. |
87(1,1,2,2) | Details |
12180978 | Kotlyar AB, Borovok N: oxidation and NAD+ reduction catalysed by tightly coupled inside-out vesicles from Paracoccus denitrificans. Biochim Biophys Acta. 1998 Jul 20;1365(3):443-52. Inhibition of the bacterial complex I by a specific inhibitor of Q reduction, rotenone, is very different from that of the mitochondrial enzyme. |
83(1,1,1,3) | Details |
17705834 | Jin J, Davis J, Zhu D, Kashima DT, Leroueil M, Pan C, Montine KS, Zhang J: Identification of novel proteins affected by rotenone in mitochondria of dopaminergic cells. J Bioenerg Biomembr. 2010 Mar 19. Rotenone, a specific inhibitor of mitochondrial complex I, has been shown to produce neurodegeneration in rats as well as in many cellular models that closely resemble PD. |
83(1,1,1,3) | Details |
11516165 | Zhang JG, Tirmenstein MA, Nicholls-Grzemski FA, Fariss MW: Mitochondrial electron transport inhibitors cause lipid peroxidation-dependent and -independent cell death: protective role of antioxidants. Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):2007-11. Epub 2009 Jan 27. The toxic effects of mitochondrial complex I and II inhibitors, rotenone (ROT) and thenoyltrifluoroacetone (TTFA), respectively, were dependent on oxidative stress and lipid peroxidation, while cell death induced by inhibitors of complexes III and IV, antimycin A (AA) and (CN), respectively, was caused by MMP collapse and loss of cellular ATP. |
82(1,1,1,2) | Details |
17916065 | Muller FL, Liu Y, Abdul-Ghani MA, Lustgarten MS, Bhattacharya A, Jang YC, Van Remmen H: High rates of production in skeletal-muscle mitochondria respiring on both complex I- and complex II-linked substrates. Neuroscience. 2007 Apr 25;146(1):350-65. Epub 2007 Mar 7. production with glutamate+succinate remained high even at low substrate concentrations (<1 mM), was decreased by rotenone and was completely eliminated by FCCP (carbonyl p-trifluoromethoxyphenylhydrazone), indicating that it must in large part originate from reverse-electron transfer through complex I. |
82(1,1,1,2) | Details |
11311359 | Jenner P: Parkinson's disease, pesticides and mitochondrial dysfunction. Free Radic Biol Med. 2006 Jul 1;41(1):154-64. Epub 2006 Apr 4. Selective nigral degeneration with inclusion formation provoked by systemic administration of the herbicide rotenone, through inhibition of complex I, raises the question of pesticide exposure and environmental factors in general, as a cause of Parkinson's disease (PD). |
82(1,1,1,2) | Details |
18445136 | Kilbride SM, Telford JE, Tipton KF, Davey GP: Partial inhibition of complex I activity increases Ca-independent release rates from depolarized synaptosomes. J Neurosci. 2000 Aug 1;20(15):5715-23. Following a 40% inhibition of complex I activity with rotenone, it was found that Ca (2+)-independent release of increased from synaptosomes depolarized with 4-aminopyridine. |
87(1,1,1,7) | Details |
9191778 | Carelli V, Ghelli A, Ratta M, Bacchilega E, Sangiorgi S, Mancini R, Leuzzi V, Cortelli P, Montagna P, Lugaresi E, Degli Esposti M: Leber's hereditary optic neuropathy: biochemical effect of 11778/ND4 and 3460/ND1 mutations and correlation with the mitochondrial genotype. Mol Microbiol. 2000 Jan;35(2):428-34. The enzymatic activities of mitochondrial complex I and its sensitivity to the potent inhibitors rotenone and rolliniastatin-2 were studied in mitochondrial particles from platelets, in correlation with mtDNA analysis of platelets and leukocytes. |
87(1,1,2,2) | Details |
11854175 | Wong A, Cavelier L, Collins-Schramm HE, Seldin MF, McGrogan M, Savontaus ML, Cortopassi GA: Differentiation-specific effects of LHON mutations introduced into neuronal NT2 cells. Hum Mol Genet. 2002 Feb 15;11(4):431-8. Differentiation of the cells to the neuronal form also resulted in significant increases in ROS production in the LHON-NT2 neurons versus controls, which is abolished by rotenone, a specific inhibitor of Complex I. |
83(1,1,1,3) | Details |
411483 | Crowder SE, Ragan CI: Effects of proteolytic digestion by chymotrypsin on the structure and catalytic properties of heart mitochondria. Biochem J. 1978 Sep 15;174(3):783-90. Incubation of NADH-ubiquinone oxidoreductase (Complex I) with chymotrypsin caused loss of rotenone-sensitive reduction and an increase in rotenone-insensitive reduction. 2. |
- oxidoreductase from bovine 83(1,1,1,3) | Details |
18436790 | Zmijewski JW, Lorne E, Zhao X, Tsuruta Y, Sha Y, Liu G, Siegal GP, Abraham E: Mitochondrial respiratory complex I regulates neutrophil activation and severity of lung injury. Br J Pharmacol. 2007 Apr;150(8):1031-43. Epub 2007 Mar 5. MEASUREMENTS AND MAIN RESULTS: Inhibition of complex I with either rotenone or the antihyperglycemic agent was associated with increased intracellular levels of both and peroxide, as well as inhibition of LPS-induced I kappaB-alpha degradation, NF-kappaB nuclear accumulation, and proinflammatory cytokine production. |
196(2,3,3,6) | Details |
12628295 | Farge G, Touraille S, Debise R, Alziari S: The respiratory chain complex thresholds in mitochondria of a Drosophila subobscura mutant strain. Can J Microbiol. 2006 Apr;52(4):317-27. Complex I, III and IV activities were inhibited by rotenone, antimycin and KCN, respectively. |
86(1,1,1,6) | Details |
12485407 | Sipos I, Tretter L, Adam-Vizi V: Quantitative relationship between inhibition of respiratory complexes and formation of reactive species in isolated nerve terminals. Autoimmunity. 1999;30(1):43-51. For inhibition of complex I, III and IV, rotenone, antimycin and were used, respectively, and ROS formation was followed by measuring the activity of aconitase enzyme. |
85(1,1,1,5) | Details |
19416678 | Belcastro V, Tozzi A, Tantucci M, Costa C, Di Filippo M, Autuori A, Picconi B, Siliquini S, Luchetti E, Borsini F, Calabresi P: A2A receptor antagonists protect the striatum against rotenone-induced neurotoxicity. Biochem Biophys Res Commun. 1993 Feb 15;190(3):1090-6. Thus, utilizing extracellular and intracellular recordings from corticostriatal brain slices, we have tested the possible neuroprotective action of two A2A receptor antagonists, ST1535 and ZM241385, on the irreversible electrophysiological effects induced by the acute application of rotenone, a pesticide acting as a selective inhibitor of mitochondrial complex I activity. |
83(1,1,1,3) | Details |
16439141 | Betarbet R, Canet-Aviles RM, Sherer TB, Mastroberardino PG, McLendon C, Kim JH, Lund S, Na HM, Taylor G, Bence NF, Kopito R, Seo BB, Yagi T, Yagi A, Klinefelter G, Cookson MR, Greenamyre JT: Intersecting pathways to neurodegeneration in Parkinson's disease: effects of the pesticide rotenone on DJ-1, alpha-synuclein, and the ubiquitin-proteasome system. Exp Neurol. 2004 Apr;186(2):235-41. To further evaluated PD pathogenesis here, we used in vivo and in vitro models of chronic low-grade complex I inhibition with the pesticide rotenone. |
83(1,1,1,3) | Details |
9237684 | Genova ML, Bovina C, Marchetti M, Pallotti F, Tietz C, Biagini G, Pugnaloni A, Viticchi C, Gorini A, Villa RF, Lenaz G: Decrease of rotenone inhibition is a sensitive parameter of complex I damage in brain non-synaptic mitochondria of aged rats. Biochem Pharmacol. 2002 Apr 1;63(7):1259-72. |
193(2,3,3,3) | Details |
12840017 | Chen Q, Vazquez EJ, Moghaddas S, Hoppel CL, Lesnefsky EJ: Production of reactive species by mitochondria: central role of complex III. Antioxid Redox Signal. 2008 Aug;10(8):1435-47. In contrast to intact mitochondria, blockade of complex I with rotenone markedly increased H2O2 production from submitochondrial particles oxidizing the complex I substrate |
166(2,2,2,6) | Details |
16141438 | Richardson JR, Quan Y, Sherer TB, Greenamyre JT, Miller GW: Paraquat neurotoxicity is distinct from that of MPTP and rotenone. . Synapse. 2010 Mar;64(3):241-50. We have also demonstrated the requirement for complex I inhibition and oxidative damage in the dopaminergic neurodegeneration produced by rotenone. |
163(2,2,2,3) | Details |
16895522 | Sherwood S, Hirst J: Investigation of the mechanism of translocation by NADH:ubiquinone oxidoreductase (complex I) from bovine heart mitochondria: does the enzyme operate by a Q-cycle mechanism?. Arch Biochem Biophys. 1997 Jan 1;337(1):69-74. Unexpectedly, in the presence of complex I inhibited by either rotenone or piericidin A was found to catalyse the exchange of redox states between different and species, providing a possible route for future investigations into the mechanism of energy transduction. |
85(1,1,1,5) | Details |
8126004 | Alves PC, Videira A: Disruption of the gene coding for the 21.3-kDa subunit of the peripheral arm of complex I from Neurospora crassa. J Neurosci. 2003 Jul 16;23(15):6181-7. We observed similar rates of rotenone-sensitive NADH:ubiquinone oxido-reductase activity in mitochondrial membranes from the mutant and wild-type strains and discuss the possibility that this electron transfer is independent of the more hydrophobic part of complex I. |
85(1,1,1,5) | Details |
15906144 | Ohnishi ST, Ohnishi T, Muranaka S, Fujita H, Kimura H, Uemura K, Yoshida K, Utsumi K: A possible site of complex I segment of rat heart mitochondria. J Neurosci. 2009 Jul 15;29(28):9002-10. In the forward electron transfer, a slow production in the presence of and was enhanced by both rotenone and piericidin A (specific inhibitors at the end of the complex I respiratory chain). |
generation in the 83(1,1,1,3) | Details |
16962686 | Biehlmaier O, Alam M, Schmidt WJ: A rat model of Parkinsonism shows depletion of in the retina. . Eur J Biochem. 1999 Oct 1;265(1):86-93. Systemic inhibition of complex I (rotenone) in rats has been proposed as a model of PD. |
163(2,2,2,3) | Details |
12496265 | Li N, Ragheb K, Lawler G, Sturgis J, Rajwa B, Melendez JA, Robinson JP: Mitochondrial complex I inhibitor rotenone induces apoptosis through enhancing mitochondrial reactive species production. Acta Pharmacol Sin. 2004 Mar;25(3):385-9. Inhibition of mitochondrial respiratory chain complex I by rotenone had been found to induce cell death in a variety of cells. |
162(2,2,2,2) | Details |
17611283 | Yadava N, Nicholls DG: Spare respiratory capacity rather than oxidative stress regulates inhibition of mitochondrial complex I with rotenone. Mol Cancer Res. 2007 Sep;5(9):923-32. |
excitotoxicity after partial respiratory 162(2,2,2,2) | Details |
10426140 | Cock HR, Cooper JM, Schapira AH: Functional consequences of the 3460-bp mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy. J Biochem. 1997 Apr;121(4):746-55. A 60% rotenone-induced decrease in complex I activity was shown to reduce ATP synthesis in normal fibroblasts, indicating that this level of complex I activity was below the threshold required to affect ATP synthesis. |
85(1,1,1,5) | Details |
9096412 | Gutierres S, Sabar M, Lelandais C, Chetrit P, Diolez P, Degand H, Boutry M, Vedel F, de Kouchkovsky Y, De Paepe R: Lack of mitochondrial and nuclear-encoded subunits of complex I and alteration of the respiratory chain in Nicotiana sylvestris mitochondrial deletion mutants. Neurosci Lett. 1995 Feb 17;186(2-3):99-102. The remaining activity was much less sensitive to rotenone, indicating the breakdown of Complex I activity. |
85(1,1,1,5) | Details |
11798025 | Greenamyre JT, Sherer TB, Betarbet R, Panov AV: Complex I and Parkinson's disease. Brain Res Bull. 2010 Mar 16;81(4-5):484-90. Epub 2009 Oct 23. Recent experimental work has modeled this abnormality using rotenone to systemically inhibit complex I. |
85(1,1,1,5) | Details |
20100453 | Batista AP, Fernandes AS, Louro RO, Steuber J, Pereira MM: Energy conservation by Rhodothermus marinus respiratory complex I. . J Neurochem. 2003 Mar;84(5):1193-200. Specific inhibitors of complex I (rotenone) and of the dioxygen reductase (KCN) inhibited the and the transport, but the KCN effect was totally reverted by the addition of analogues, indicating that both transports were catalyzed by complex I. |
83(1,1,1,3) | Details |
10386974 | Chinopoulos C, Tretter L, Adam-Vizi V: Depolarization of in situ mitochondria due to peroxide-induced oxidative stress in nerve terminals: inhibition of alpha-ketoglutarate dehydrogenase. PLoS One. 2009;4(1):e4250. Epub 2009 Jan 22. When complex I of the respiratory chain was inhibited by rotenone (2 microM), delta psi (m) was unaltered, but on subsequent addition of H2O2, delta psi (m) started to decrease and collapsed during incubation with 0.5 mM H2O2 for 12 min. |
83(1,1,1,3) | Details |
11299009 | Bykova NV, Moller IM: Involvement of matrix oxidation of NAD-linked substrates by pea leaf mitochondria. Plant Physiol. 1990 Sep;94(1):189-193. As estimated by the inhibition caused by 5 microM diphenyleneiodonium (DPI) in the presence of rotenone to inhibit complex I, the activity of NDin during oxidation (measured both as O2 uptake and as CO2 release) was 40-50 nmol mg-1 protein min-1. |
turnover in the 162(2,2,2,2) | Details |
12177198 | Sherer TB, Betarbet R, Stout AK, Lund S, Baptista M, Panov AV, Cookson MR, Greenamyre JT: An in vitro model of Parkinson's disease: linking mitochondrial impairment to altered alpha-synuclein metabolism and oxidative damage. Sleep. 2007 Apr 1;30(4):413-25. Chronic systemic complex I inhibition caused by rotenone exposure induces features of Parkinson's disease (PD) in rats, including selective nigrostriatal dopaminergic degeneration and formation of ubiquitin- and alpha-synuclein-positive inclusions (Betarbet et al., 2000). |
162(2,2,2,2) | Details |
12411515 | Hanley PJ, Ray J, Brandt U, Daut J: Halothane, isoflurane and sevoflurane inhibit NADH:ubiquinone oxidoreductase (complex I) of cardiac mitochondria. Biochim Biophys Acta. 1993 Mar 1;1141(2-3):262-8. Unlike the classical inhibitor rotenone, none of the anaesthetics completely inhibited enzyme activity at high concentration, suggesting that these agents bind weakly to the 'hydrophobic inhibitory site' of complex I. |
85(1,1,1,5) | Details |
18358763 | Dlaskova A, Hlavata L, Jezek J, Jezek P: Mitochondrial Complex I production is attenuated by uncoupling. Antioxid Redox Signal. 2005 Sep-Oct;7(9-10):1110-6. It also partially prevented suppression by FCCP of rotenone-induced H (2) O (2) production with Complex I substrates alone and but nearly completely with Complexes I and II substrates. |
85(1,1,1,5) | Details |
18077608 | Chen Q, Moghaddas S, Hoppel CL, Lesnefsky EJ: Ischemic defects in the electron transport chain increase the production of reactive species from isolated rat heart mitochondria. Physiol Plant. 2004 Mar;120(3):370-385. Inhibition of complex I with rotenone increased H (2) O (2) production by 179 +/- 24% and 155 +/- 14% in SSM and IFM, respectively, following ischemia. |
83(1,1,1,3) | Details |
9593904 | Degli Esposti M: Inhibitors of -ubiquinone reductase: an overview. Hum Mol Genet. 2004 Apr 1;13(7):669-81. Epub 2004 Feb 12. The inhibitors are presented within the broad categories of natural and commercial compounds and their potency is related to that of rotenone, the classical inhibitor of complex I. |
83(1,1,1,3) | Details |
9131045 | Grivennikova VG, Maklashina EO, Gavrikova EV, Vinogradov AD: Interaction of the mitochondrial -ubiquinone reductase with rotenone as related to the enzyme active/inactive transition. J Biol Chem. 1994 Aug 19;269(33):21037-42. The interaction of rotenone with active ('pulsed') and thermally de-activated ('resting') membrane-bound Complex I (Kotlyar, A.B. and Vinogradov, A.D. (1990) Biochim. |
162(2,2,2,2) | Details |
15347666 | Lesnefsky EJ, Chen Q, Moghaddas S, Hassan MO, Tandler B, Hoppel CL: Blockade of electron transport during ischemia protects cardiac mitochondria. Neurobiol Dis. 2009 Feb;33(2):182-92. Epub 2008 Oct 26. Isolated, perfused rabbit hearts were treated with rotenone, an irreversible inhibitor of complex I in the proximal electron transport chain, immediately before ischemia. |
162(2,2,2,2) | Details |
7735172 | Charalambous A, Mangner TJ, Kilbourn MR: Synthesis of (2-[11C] methoxy) rotenone, a marker of mitochondrial complex I activity. Neuropharmacology. 2008 Dec;55(8):1340-6. Epub 2008 Sep 10. Rotenone is a potent reversible competitive inhibitor of complex I - reductase). |
143(1,3,3,3) | Details |
9684860 | Darrouzet E, Issartel JP, Lunardi J, Dupuis A: The 49-kDa subunit of NADH-ubiquinone oxidoreductase (Complex I) is involved in the binding of piericidin and rotenone, two -related inhibitors. Chem Biol Interact. 2001 Dec 21;138(3):267-84. |
84(1,1,1,4) | Details |
16584707 | Borutaite V, Brown GC: S-nitrosothiol inhibition of mitochondrial complex I causes a reversible increase in mitochondrial peroxide production. Biochim Biophys Acta. 2006 May-Jun;1757(5-6):562-6. Epub 2006 Mar 23. Specific inhibition of complex I with rotenone increased H2O2 production to a similar extent as that caused by SNAP. |
84(1,1,1,4) | Details |
16678117 | Grivennikova VG, Vinogradov AD: Generation of Complex I. . Plant Physiol. 2000 Nov;124(3):1239-50. The -supported production was inhibited by rotenone and uncouplers, showing that most part of produced during oxidation is originated from univalent reduction by Complex I. |
by the mitochondrial 83(1,1,1,3) | Details |
11245783 | Prieur I, Lunardi J, Dupuis A: Evidence for a binding site close to the interface between NUOD and NUOB subunits of Complex I. FEBS Lett. 1999 May 28;451(3):347-50. Piericidin, rotenone and pyridaben are specific inhibitors of the NADH-ubiquinone oxidoreductase (Complex I) that bind to its binding site (s). |
83(1,1,1,3) | Details |
1521539 | Menz RI, Griffith M, Day DA, Wiskich JT: Matrix NADH dehydrogenases of plant mitochondria and sites of reduction by complex I. Ann Neurol. 1991 Nov;30(5):701-8. We confirm that there are two dehydrogenases capable of oxidising internal and that only one of these, namely complex I, is inhibited by rotenone. |
119(1,2,3,4) | Details |
15571245 | Gattermann N, Dadak M, Hofhaus G, Wulfert M, Berneburg M, Loeffler ML, Simmonds HA: Severe impairment of nucleotide synthesis through inhibition of mitochondrial respiration. Eur J Biochem. 1994 Nov 15;226(1):237-42. This was surprising since Rotenone inhibits complex I of the respiratory chain, which is upstream of where DHODH interacts with the RC. |
118(1,2,3,3) | Details |
8656275 | Higgins DS Jr, Greenamyre JT: [3H] dihydrorotenone binding to ubiquinone reductase (complex I) of the electron transport chain: an autoradiographic study. Exp Parasitol. 2002 Jan;100(1):54-61. In skeletal muscle, heart, and kidney, binding was less affected by [3H] DHR binding is inhibited by rotenone (IC50 = 8-20 nM), meperidine (IC50 = 34-57 microM), amobarbitol (IC50 = 375-425 microM), and MPP+ (IC50 = 4-5 mM), consistent with the potencies of these compounds in inhibiting complex I activity. |
117(1,2,2,7) | Details |
17477844 | Zoccarato F, Cavallini L, Bortolami S, Alexandre A: modulation of H2O2 release at NADH:ubiquinone oxidoreductase (Complex I) in brain mitochondria. Biochem Biophys Res Commun. 2009 Oct 16;388(2):311-6. Epub 2009 Aug 5. The much faster -dependent H2O2 production is ascribed to Complex I, being rotenone-sensitive. |
84(1,1,1,4) | Details |
7649309 | Vinogradov AD, Sled VD, Burbaev DS, Grivennikova VG, Moroz IA, Ohnishi T: Energy-dependent Complex I-associated ubisemiquinones in submitochondrial particles. Chem Biol Interact. 1995 Oct 20;98(1):1-13. The g = 2.00 signals from both fast-relaxing SQNf (P1/2 = 170 mW at 40 K) and slow-relaxing SQNs (P1/2 = 0.7 mW) are sensitive to uncouplers, rotenone and thermally induced deactivation of Complex I. |
84(1,1,1,4) | Details |
12237311 | St-Pierre J, Buckingham JA, Roebuck SJ, Brand MD: Topology of production from different sites in the mitochondrial electron transport chain. FEBS Lett. 1995 Aug 14;370(1-2):83-7. However, when complex I was fully reduced using rotenone, rat mitochondria released significantly more peroxide than pigeon mitochondria. |
84(1,1,1,4) | Details |
18615133 | Bonsi P, Cuomo D, Martella G, Sciamanna G, Tolu M, Calabresi P, Bernardi G, Pisani A: Mitochondrial toxins in Basal Ganglia disorders: from animal models to therapeutic strategies. J Am Soc Nephrol. 2002 May;13(5):1179-89. MPTP and rotenone, both selective inhibitors of mitochondrial complex I have been extensively used to mimic PD. |
82(1,1,1,2) | Details |
16120427 | Blanco FJ, Lopez-Armada MJ, Maneiro E: Mitochondrial dysfunction in osteoarthritis. . Mitochondrion. 2004 Sep;4(5-6):715-28. Epub 2004 Oct 1. Inhibition of complex I with rotenone increases the expression and synthesis of Bcl-2 and Cox-2, both effects are similar effects to produced by IL-1 in human chondrocytes. |
82(1,1,1,2) | Details |
11146003 | Chinopoulos C, Adam-Vizi V: Mitochondria deficient in complex I activity are depolarized by peroxide in nerve terminals: relevance to Parkinson's disease. Ann Neurol. 1999 Mar;45(3):320-8. Here we demonstrate that the membrane potential of in situ mitochondria (Delta Psi m), as measured by the fluorescence change of JC-l (5,5',6,6'-tetrachloro-1,1,3,3'-tetraethylbezimidazolyl-carbocyani ne iodide), collapses when isolated nerve terminals are exposed to peroxide (H (2) O (2), 100 and 500 microM) in combination with the inhibition of complex I by rotenone (5 nM-1 microM). |
116(1,2,2,6) | Details |
9832155 | Hensley K, Pye QN, Maidt ML, Stewart CA, Robinson KA, Jaffrey F, Floyd RA: Interaction of alpha-phenyl-N-tert-butyl nitrone and alternative electron acceptors with complex I indicates a substrate reduction site upstream from the rotenone binding site. J Neural Transm Suppl. 2006;(70):273-6. |
115(1,2,2,5) | Details |
19233273 | Silva JM, Wong A, Carelli V, Cortopassi GA: Inhibition of mitochondrial function induces an integrated stress response in oligodendroglia. J Biol Chem. 2003 Sep 26;278(39):37832-9. Epub 2003 Jul 9. Therefore, we wanted to determine whether mitochondrial dysfunction induced by complex I inhibition with rotenone can activate the ISR, specifically by the ER kinase PERK, in oligodendroglial cells. |
84(1,1,1,4) | Details |
15175007 | Lambert AJ, Brand MD: production by NADH:ubiquinone oxidoreductase (complex I) depends on the pH gradient across the mitochondrial inner membrane. Planta. 2006 Jun;224(1):196-204. Epub 2006 Jan 17. By far, the largest rate of production was from mitochondria respiring on this rate was almost abolished by rotenone or piericidin, indicating that production from complex I is large under conditions of reverse electron transport. |
84(1,1,1,4) | Details |
19664596 | Ota S, Horigome K, Ishii T, Nakai M, Hayashi K, Kawamura T, Kishino A, Taiji M, Kimura T: suppresses glucose-6-phosphatase expression by a complex I inhibition and AMPK activation-independent mechanism. Neurochem Res. 2009 Jun 4. Since NDI1 can functionally complement the complex I under the presence of or rotenone, our results indicate that induces down-regulation of G6pc expression through an inhibition of complex I and an activation of AMPK-independent mechanism. |
83(1,1,1,3) | Details |
11936880 | Gschwend MH, Rudel R, Strauss WS, Sailer R, Brinkmeier H, Schneckenburger H: Optical detection of mitochondrial In the absence of the fluorescent mitochondrial marker rhodamine (R123), the autofluorescence (i.e. a signal monitoring cytoplasmic plus mitochondrial remained unchanged upon inhibition of complex I by rotenone, and was increased by a factor of 2 upon inhibition of complex III by antimycin. |
content in intact human myotubes. Cell Mol Biol (Noisy-le-grand). 2001;47 Online Pub:OL95-104.82(1,1,1,2) | Details |
20143419 | Corona JC, Gimenez-Cassina A, Lim F, Diaz-Nido J: Hexokinase II gene transfer protects against neurodegeneration in the rotenone and MPTP mouse models of Parkinson's disease. J Neurosci Res. 2010 Feb 8. Rotenone or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) inhibit the mitochondrial complex I and they cause the death of substantia nigra dopaminergic neurons, thereby providing acute murine models of Parkinson's disease. |
82(1,1,1,2) | Details |
16543240 | Seo BB, Nakamaru-Ogiso E, Flotte TR, Matsuno-Yagi A, Yagi T: In vivo complementation of complex I by the yeast Ndi1 enzyme. J Neurol Sci. 2004 Aug 30;223(2):149-55. We have shown previously that the single subunit rotenone-insensitive -quinone oxidoreductase (Ndi1) of Saccharomyces cerevisiae mitochondria can restore oxidation in complex I-deficient mammalian cells. |
115(1,2,2,5) | Details |
11997134 | Ventura B, Genova ML, Bovina C, Formiggini G, Lenaz G: Control of oxidative phosphorylation by Complex I in rat liver mitochondria: implications for aging. J Bioenerg Biomembr. 1995 Aug;27(4):397-406. This indication was strengthened by examining the rotenone inhibition thresholds showing that Complex I becomes more rate controlling, over all the examined activities, during aging. |
115(1,2,2,5) | Details |
10652103 | Steuber J, Schmid C, Rufibach M, Dimroth P: Na+ translocation by complex I (NADH:quinone oxidoreductase) of Escherichia coli. Biofactors. 2008;32(1-4):31-9. With an E. coli mutant deficient in complex I, the Na+ transport activity was low (1-3 nmol mg-1 min-1), and rotenone was without effect. |
115(1,2,2,5) | Details |
8769881 | Morikawa N, Nakagawa-Hattori Y, Mizuno Y: Effect of papaverine, and related compounds on mitochondrial respiration and complex I activity. Biochim Biophys Acta. 2007 May;1772(5):533-42. Epub 2007 Jan 26. Papaverine was the most potent inhibitor of complex I and -linked mitochondrial respiration among the compounds tested next to rotenone. |
dimethoxyphenylethylamine, 84(1,1,1,4) | Details |
17540903 | Reeves MB, Davies AA, McSharry BP, Wilkinson GW, Sinclair JH: Complex I binding by a virally encoded RNA regulates mitochondria-induced cell death. Biochemistry. 2003 Mar 18;42(10):3032-9. Using rotenone, a potent inhibitor of the mitochondrial enzyme complex I - oxido-reductase), we found that human cytomegalovirus infection protected cells from rotenone-induced apoptosis, a protection mediated by a 2.7-kilobase virally encoded RNA (beta2.7). |
84(1,1,1,4) | Details |
10371157 | Galkin AS, Grivennikova VG, Vinogradov AD: --> H+/2e- stoichiometry in quinone reductase reactions catalyzed by bovine heart submitochondrial particles. Biochemistry. 2007 Sep 25;46(38):10971-8. Epub 2007 Aug 31. Rotenone, piericidin and thermal deactivation of complex I completely prevented -induced translocation in the -endogenous ubiquinone reductase reaction. |
-82(1,1,1,2) | Details |
20300811 | Sanz A, Stefanatos R, McIlroy G: Production of reactive species by the mitochondrial electron transport chain in Drosophila melanogaster. Toxicol Sci. 2005 Nov;88(1):193-201. Epub 2005 Sep 1. The production of ROS during reverse electron transport can be prevented either by rotenone or by the oxidation of by complex I. |
82(1,1,1,2) | Details |
15790535 | Testa CM, Sherer TB, Greenamyre JT: Rotenone induces oxidative stress and dopaminergic neuron damage in organotypic substantia nigra cultures. Biochim Biophys Acta. 1999 Jan 6;1453(1):49-62. Chronic complex I inhibition over weeks by low dose (10-50 nM) rotenone in this system lead to dose- and time-dependent destruction of substantia nigra pars compacta neuron processes, morphologic changes, some neuronal loss, and decreased tyrosine hydroxylase (TH) protein levels. |
114(1,2,2,4) | Details |
14570403 | Sipos I, Tretter L, Adam-Vizi V: The production of reactive species in intact isolated nerve terminals is independent of the mitochondrial membrane potential. Toxicol Sci. 2007 Jan;95(1):163-71. Epub 2006 Oct 3. In addition, we detected a significant antimycin-induced H2O2 production when the flow of electrons through complex I was inhibited by rotenone, indicating that the respiratory chain of in situ mitochondria in synaptosomes has a substantial electron influx distal from the rotenone site, which could contribute to ROS generation when the complex III is inhibited. |
114(1,2,2,4) | Details |
11164812 | Sherer TB, Trimmer PA, Borland K, Parks JK, Bennett JP Jr, Tuttle JB: Chronic reduction in complex I function alters signaling in SH-SY5Y neuroblastoma cells. Brain Res. 2000 Jun 23;868(2):191-201. A pharmacological model of reduced complex I activity was created by prolonged treatment of SH-SY5Y cells with low doses (5-20 nM) of rotenone, a selective inhibitor of complex I. |
84(1,1,1,4) | Details |
3132077 | Ichiki T, Tanaka M, Nishikimi M, Suzuki H, Ozawa T, Kobayashi M, Wada Y: Deficiency of subunits of Complex I and mitochondrial encephalomyopathy. . Am J Physiol Cell Physiol. 2005 Jun;288(6):C1440-50. Epub 2005 Jan 12. In all patients, the content of subunits of Complex I was also reduced in parallel with the rotenone-sensitive -cytochrome c reductase activity. |
84(1,1,1,4) | Details |
18032788 | Chen Y, McMillan-Ward E, Kong J, Israels SJ, Gibson SB: Mitochondrial electron-transport-chain inhibitors of complexes I and II induce autophagic cell death mediated by reactive species. Biochim Biophys Acta. 2007 Mar;1767(3):222-32. Epub 2007 Feb 9. Herein, we determined that inhibitors of complex I (rotenone) and complex II (TTFA) induce cell death and autophagy in the transformed cell line HEK 293, and in cancer cell lines U87 and HeLa. |
82(1,1,1,2) | Details |
8313963 | Finel M, Majander A: Studies on the NADH:ubiquinone oxidoreductases of mitochondria and Escherichia coli using the inhibitor 1,10-phenanthroline. Brain Res. 1997 Feb 21;749(1):44-52. EPR spectroscopy of submitochondrial particles indicates that OP, similarly to rotenone, inhibits electron transfer between the Fe-S clusters of complex I and the pool. |
-translocating 82(1,1,1,2) | Details |
19073440 | King TD, Clodfelder-Miller B, Barksdale KA, Bijur GN: Unregulated mitochondrial GSK3beta activity results in Conversely, chemical inhibitors of GSK3beta inhibited MPP+- and rotenone-induced apoptosis, and attenuated the mitochondrial GSK3beta-mediated impairment in complex I. |
oxidoreductase deficiency. Am J Physiol Cell Physiol. 2008 Apr;294(4):C945-56. Epub 2008 Jan 30.113(1,2,2,3) | Details |
18784283 | Garmier M, Carroll AJ, Delannoy E, Vallet C, Day DA, Small ID, Millar AH: Complex I dysfunction redirects cellular and mitochondrial metabolism in Arabidopsis. Plant Physiol. 2008 Nov;148(3):1324-41. Epub 2008 Sep 10. These data demonstrate that, in Arabidopsis cells, complex I inhibition by rotenone induces significant remodeling of metabolic pathways involving the mitochondria and other compartments and point to early metabolic changes in response to mitochondrial dysfunction. |
113(1,2,2,3) | Details |
8037664 | Degli Esposti M, Ghelli A, Ratta M, Cortes D, Estornell E: Natural substances (acetogenins) from the family Annonaceae are powerful inhibitors of mitochondrial NADH dehydrogenase (Complex I). Front Biosci. 2007 Jan 1;12:1079-93. The properties of five of such acetogenins are compared with those of rotenone and piericidin, classical potent inhibitors of Complex I. |
84(1,1,1,4) | Details |
15836612 | Votyakova TV, Reynolds IJ: Ca2+-induced permeabilization promotes free radical release from rat brain mitochondria with partially inhibited complex I. Mol Biochem Parasitol. 1994 Mar;64(1):87-94. In this study we investigated the effect of Ca2+ loads on ROS release from rat brain mitochondria with complex I partially inhibited by rotenone. |
84(1,1,1,4) | Details |
12753929 | Sousa SC, Maciel EN, Vercesi AE, Castilho RF: Ca2+-induced oxidative stress in brain mitochondria treated with the respiratory chain inhibitor rotenone. FEBS Lett. 2003 May 22;543(1-3):179-83. Ca (2+)-stimulated mitochondrial ROS release was associated with membrane lipid peroxidation and was directly correlated with the degree of complex I inhibition by rotenone. |
82(1,1,1,2) | Details |
2128595 | Wijburg FA, Feller N, de Groot CJ, Wanders RJ: oxidation and -synthesis in complex I deficient fibroblasts. Neurosci Lett. 2003 Nov 6;351(1):29-32. In this paper we report our studies on the effects of in cultured fibroblasts treated with rotenone to block complex I. |
partially restores -82(1,1,1,2) | Details |
16219024 | Hoglinger GU, Lannuzel A, Khondiker ME, Michel PP, Duyckaerts C, Feger J, Champy P, Prigent A, Medja F, Lombes A, Oertel WH, Ruberg M, Hirsch EC: The mitochondrial complex I inhibitor rotenone triggers a cerebral tauopathy. Eur J Biochem. 1994 Jan 15;219(1-2):691-8. To determine experimentally whether chronic generalized complex I inhibition has an effect on the distribution of alpha-synuclein or tau, we infused rats systemically with the plant-derived isoflavonoid rotenone. |
113(1,2,2,3) | Details |
11677254 | Votyakova TV, Reynolds IJ: DeltaPsi (m)-Dependent and -independent production of reactive species by rat brain mitochondria. Neurobiol Dis. 2006 May;22(2):404-20. Epub 2006 Jan 24. Mitochondria respiring on the complex I substrates, and produce very little ROS until complex I is inhibited with rotenone, which is also consistent with complex I being the major site of ROS generation. |
113(1,2,2,3) | Details |
17011837 | Bacsi A, Woodberry M, Widger W, Papaconstantinou J, Mitra S, Peterson JW, Boldogh I: Localization of production to mitochondrial electron transport chain in 3-NPA-treated cells. Biochem J. 1979 Aug 15;182(2):353-60. In the present study, we identified the site of reactive species production in mitochondria. 3-NPA increased O2- generation in mitochondria respiring on the complex I substrates pyruvate+malate, an effect fully inhibited by rotenone. |
84(1,1,1,4) | Details |
17702527 | Coe KJ, Jia Y, Ho HK, Rademacher P, Bammler TK, Beyer RP, Farin FM, Woodke L, Plymate SR, Fausto N, Nelson SD: Comparison of the cytotoxicity of the nitroaromatic drug flutamide to its cyano analogue in the hepatocyte cell line TAMH: evidence for complex I inhibition and mitochondrial dysfunction using toxicogenomic screening. Free Radic Biol Med. 2003 Jul 1;35(1):24-32. Comparisons of transcriptomic changes caused by FLU with those caused by a panel of known cytotoxicants tetrafluoroethylcysteine, diquat, and rotenone (ROT)] indicated that FLU results in a temporal gene expression pattern similar to ROT, a known inhibitor of complex I of the electron transport chain. |
84(1,1,1,4) | Details |
17320357 | Park JS, Li YF, Bai Y: Yeast NDI1 improves oxidative phosphorylation capacity and increases protection against oxidative stress and cell death in cells carrying a Leber's hereditary optic neuropathy mutation. Arterioscler Thromb Vasc Biol. 2003 Oct 1;23(10):1754-60. Epub 2003 Sep 4. In transformant cell lines, LeNDI1-1 and -2, total and complex I-dependent respiration were fully restored and largely resistant to complex I inhibitor, rotenone, indicating a dominant role of NDI1 in the transfer of electrons in the host cells. |
82(1,1,1,2) | Details |
11346950 | Zhang Q, Soole KL, Wiskich JT: Regulation of respiration in rotenone-treated tobacco cell suspension cultures. Eur J Biochem. 1994 Jun 15;222(3):975-82. Cells of Nicotiana tabacum L. suspension cultures were treated with the respiratory inhibitor rotenone, which specifically inhibits complex I activity of mitochondria. |
82(1,1,1,2) | Details |
10854571 | Lamensdorf I, Eisenhofer G, Harvey-White J, Nechustan A, Kirk K, Kopin IJ: 3,4-Dihydroxyphenylacetaldehyde potentiates the toxic effects of metabolic stress in PC12 cells. Cell Death Differ. 2005 Nov;12(11):1417-28. Here, we examined the potential role of DOPAL in the toxicity induced by complex I inhibition in PC12 cells and compared the effects of rotenone on concentrations of DOPAL and DOPET to those of MPP (+). |
113(1,2,2,3) | Details |
17127363 | Gomez C, Bandez MJ, Navarro A: Pesticides and impairment of mitochondrial function in relation with the parkinsonian syndrome. Eur J Neurosci. 2005 Jul;22(1):125-32. The determination of -cytochrome c reductase, -cytochrome c reductase and cytochrome oxidase activities in rat brain submitochondrial showed again the selective inhibition of Complex I by rotenone and pyridaben, whereas paraquat produced a non-selective inhibition affecting all the respiratory chain complexes. |
113(1,2,2,3) | Details |
1497345 | Bironaite DA, Cenas NK, Anusevicius ZJ, Medentsev AG, Akimenko VK, Usanov SA: Fungal inhibitors of mitochondrial NADH:ubiquinone reductase. FEBS Lett. 1998 Jul 10;431(1):34-8. The bimolecular rate constants (turnover number (TN)/Km) of rotenone-insensitive reduction of these compounds are in the range of 1.2 x 10 (4)-1.6 x 10 (5) M-1s-1. 2-Oxyjuglone acts as inhibitor of NADH:ferricyanide reductase reaction of complex I (KI = 30 microM). |
pigments as oxidizers and 83(1,1,1,3) | Details |
16234867 | Chen Y, Suzuki I: Effects of electron transport inhibitors and uncouplers on the oxidation of ferrous iron and compounds interacting with ferric iron in Acidithiobacillus ferrooxidans. Am J Respir Crit Care Med. 1995 Jun;151(6):1848-51. The oxidation rates of Fe2+ and inhibited by complex I and complex III inhibitors (amytal, rotenone, antimycin A, myxothiazol, and HQNO) were stimulated more extensively by uncouplers than the control rates. |
83(1,1,1,3) | Details |
18639366 | Jia H, Liu Z, Li X, Feng Z, Hao J, Li X, Shen W, Zhang H, Liu J: Synergistic anti-Parkinsonism activity of high doses of B vitamins in a chronic cellular model. J Biol Chem. 2006 Apr 14;281(15):10143-52. Epub 2006 Jan 12. Pretreatment with B vitamins (also 4 weeks) prevented rotenone-induced: (1) mitochondrial dysfunction, including reduced mitochondrial membrane potential and activities of complex I; (2) oxidative stress, including increase in reactive species, oxidative DNA damage and protein oxidation, and (3) Parkinsonism parameters, including accumulation of alpha-synuclein and poly-ubiquitin. |
82(1,1,1,2) | Details |
12935904 | Carriere A, Fernandez Y, Rigoulet M, Penicaud L, Casteilla L: Inhibition of preadipocyte proliferation by mitochondrial reactive species. J Child Neurol. 1991 Apr;6(2):134-42. Rotenone and oligomycin, inhibitors of complex I and of ATP synthase respectively, increased H (2) O (2) and inhibited cell growth of preadipocytes (without inducing necrosis or apoptosis). |
82(1,1,1,2) | Details |
14515342 | Leng A, Feldon J, Ferger B: Rotenone increases -induced release but does not affect -free radical formation in rat striatum. J Neurochem. 2001 Jan;76(1):302-6. To investigate the relationship of free radical formation, complex I inhibition, and release, rotenone (15 mg/kg s.c.) was injected in male Sprague Dawley rats. |
113(1,2,2,3) | Details |
9125443 | Ferrante RJ, Schulz JB, Kowall NW, Beal MF: Systemic administration of rotenone produces selective damage in the striatum and globus pallidus, but not in the substantia nigra. Arch Biochem Biophys. 2001 Sep 1;393(1):87-96. Rotenone is an insecticide which is a specific inhibitor of complex I. |
113(1,2,2,3) | Details |
15936733 | Saravanan KS, Sindhu KM, Mohanakumar KP: Acute intranigral infusion of rotenone in rats causes progressive biochemical lesions in the striatum similar to Parkinson's disease. FEBS Lett. 1991 Jul 29;286(1-2):129-32. Unilateral stereotaxic infusion of rotenone (2-12 mug in 1 mul) into substantia nigra (SN) pars compacta caused significant inhibition of complex-I activity and increased production of in vivo as measured employing spectrophotometric and HPLC-electrochemical procedures, respectively. |
112(1,2,2,2) | Details |
3691507 | Nohl H: Demonstration of the existence of an organo-specific NADH dehydrogenase in heart mitochondria. Biochem Pharmacol. 1991 Feb 15;41(4):543-52. The "exogenous NADH dehydrogenase" of heart mitochondria was found to introduce reducing equivalents into the respiratory chain before the rotenone block, indicating that the enzyme is associated with complex I. |
83(1,1,1,3) | Details |
19913015 | Costa C, Tozzi A, Luchetti E, Siliquini S, Belcastro V, Tantucci M, Picconi B, Ientile R, Calabresi P, Pisani F: Electrophysiological actions of zonisamide on striatal neurons: Selective neuroprotection against complex I mitochondrial dysfunction. Nippon Rinsho. 2002 Apr;60 Suppl 4:171-4. Thus, ZNS was also tested in two different in vitro models obtained by acutely exposing corticostriatal slices either to rotenone, a selective inhibitor of mitochondrial complex I, or to 3-nitropropionic acid (3-NP), an inhibitor of complex II. |
83(1,1,1,3) | Details |
15507238 | Li J, Fu P, French BA, French SW: The effect of rotenone on the urinary cycle in rats fed intragastrically. J Neurosci. 2002 Feb 1;22(3):782-90. Rotenone also inhibits complex I and induces a reduced state. |
82(1,1,1,2) | Details |
7926004 | Degli Esposti M, Carelli V, Ghelli A, Ratta M, Crimi M, Sangiorgi S, Montagna P, Lenaz G, Lugaresi E, Cortelli P: Functional alterations of the mitochondrially encoded ND4 subunit associated with Leber's hereditary optic neuropathy. Neurosci Lett. 2008 Dec 5;447(1):87-91. Epub 2008 Sep 24. We report that this amino acid substitution alters the affinity of complex I for the substrate and induces resistance towards its potent inhibitor rotenone in mitochondria of LHON patients. |
82(1,1,1,2) | Details |
18022104 | Yalamanchili P, Wexler E, Hayes M, Yu M, Bozek J, Kagan M, Radeke HS, Azure M, Purohit A, Casebier DS, Robinson SP: Mechanism of uptake and retention of F-18 BMS-747158-02 in cardiomyocytes: a novel PET myocardial imaging agent. Toxicol Appl Pharmacol. 1999 Aug 1;158(3):296-302. METHODS AND RESULTS: 19 BMS-747158-01 inhibited mitochondrial complex I (MC-I) in bovine heart submitochondrial particles with an IC (50) of 16.6 +/- 3 nmol/L that was comparable to the reference inhibitors of MC-1, rotenone, pyridaben, and deguelin (IC (50) of 18.2 +/- 6.7 nmol/L, 19.8 +/- 2.6 nmol/L, and 23.1 +/- 1.5 nmol/L, respectively). |
31(0,1,1,1) | Details |
11040979 | Korkisha OV, Ruuge EK: [Generation of heart mitochondria: study by spin trapping under continuous oxygenation]. J Nucl Cardiol. 2007 Nov-Dec;14(6):782-8. Epub 2007 Oct 22. The inhibition of the reverse electron transport in complex I of the respiratory chain by rotenone (oxidation substrate-- caused a substantial decrease in the rate of O2-. formation by mitochondria. |
radicals by 31(0,1,1,1) | Details |
11705700 | Frantseva MV, Carlen PL, Perez Velazquez JL: Dynamics of intracellular production during ischemia in pyramidal neurons. Neurotoxicology. 2006 Sep;27(5):826-34. Epub 2006 Apr 28. Ischemia-induced FR generation was decreased by the mitochondrial complex I blocker, rotenone, indicating that mitochondria are the principal source of ischemic FR production. |
and free radical 31(0,1,1,1) | Details |
9495873 | Brambilla L, Sestili P, Guidarelli A, Palomba L, Cantoni O: Electron transport-mediated wasteful consumption of promotes the lethal response of U937 cells to tert-butylhydroperoxide. J Biol Chem. 1994 Mar 11;269(10):7777-84. Rotenone mitigated the lethal effects of the hydroperoxide over the same concentration-range in which the complex I inhibitor inhibited utilization. |
31(0,1,1,1) | Details |
12826253 | Servais S, Couturier K, Koubi H, Rouanet JL, Desplanches D, Sornay-Mayet MH, Sempore B, Lavoie JM, Favier R: Effect of voluntary exercise on H2O2 release by subsarcolemmal and intermyofibrillar mitochondria. Mol Pharmacol. 2002 Jul;62(1):22-9. Inhibition of H (2) O (2) formation by rotenone suggests that complex I of the electron transport chain is likely the major physiological H (2) O (2)-generating system. |
31(0,1,1,1) | Details |
16313906 | Pan T, Li X, Xie W, Jankovic J, Le W: mediated Hsp70 induction and anti-apoptotic neuroprotection in SH-SY5Y cells. Chem Res Toxicol. 2007 Sep;20(9):1277-90. Epub 2007 Aug 17. We now show that attenuates rotenone (a potent complex I inhibitor)-induced apoptosis through the induction of heat shock protein 70, which may interact with apoptotic-protease-activating factor 1. |
-31(0,1,1,1) | Details |
10200266 | Au HC, Seo BB, Matsuno-Yagi A, Yagi T, Scheffler IE: The NDUFA1 gene product (MWFE protein) is essential for activity of complex I in mammalian mitochondria. Neuropharmacology. 2007 Mar;52(3):827-35. Epub 2006 Nov 22. Complementation with hamster NDUFA1 cDNA restored the rotenone-sensitive complex I activity of these mutant cells to approximately 100% of the parent cell activity. |
11(0,0,1,6) | Details |
11695833 | Yagi T, Seo BB, Di Bernardo S, Nakamaru-Ogiso E, Kao MC, Matsuno-Yagi A: NADH dehydrogenases: from basic science to biomedicine. Mol Neurobiol. 2005;31(1-3):81-93. This project involves attempting to repair complex I defects in the mammalian system using Saccharomyces cerevisiae NDI1 genes, which code for the internal, rotenone-insensitive -quinone oxidoreductase. |
10(0,0,1,5) | Details |
11124957 | Grivennikova VG, Kapustin AN, Vinogradov AD: Catalytic activity of NADH-ubiquinone oxidoreductase (complex I) in intact mitochondria. evidence for the slow active/inactive transition. J Neurochem. 2002 Aug;82(3):482-94. Alamethicin-treated mitochondria catalyzed the rotenone-sensitive -quinone reductase reaction with exogenousely added and -acceptor at the rates expected if the enzyme active sites would be freely accessible for the substrates. |
6(0,0,0,6) | Details |
12626666 | Ortega-Saenz P, Pardal R, Garcia-Fernandez M, Lopez-Barneo J: Rotenone selectively occludes sensitivity to hypoxia in rat carotid body glomus cells. Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4354-9. However, rotenone, a complex I blocker, selectively occludes the responsiveness to hypoxia of glomus cells in a dose-dependent manner. |
6(0,0,1,1) | Details |
6317663 | Kang D, Narabayashi H, Sata T, Takeshige K: Kinetics of heart mitochondria. Neuroscience. 2007 Mar 2;145(1):130-41. Epub 2007 Jan 4. Formation of anions (O2-) by bovine heart NADH-dehydrogenase preparation (Complex I) supported by an - or -generating system was studied kinetically. The plots of the -dependent activity of rotenone-treated submitochondrial particles were also biphasic. |
formation by respiratory chain - dehydrogenase of bovine 3(0,0,0,3) | Details |
18797987 | Martins VP, Soriani FM, Magnani T, Tudella VG, Goldman GH, Curti C, Uyemura SA: Mitochondrial function in the yeast form of the pathogenic fungus Paracoccidioides brasiliensis. Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2826-31. Respiration, membrane potential, and oxidative phosphorylation in mitochondria from P. brasiliensis spheroplasts were evaluated in situ, and the presence of a complete (Complex I-V) functional respiratory chain was demonstrated. The presence of an alternative NADH-ubiquinone oxidoreductase was indicated by: (i) the ability to oxidize exogenous and (ii) the lack of sensitivity to rotenone and presence of sensitivity to |
3(0,0,0,3) | Details |
11403652 | Galkin AS, Grivennikova VG, Vinogradov AD: H+/2e- stoichiometry of the nadh:ubiquinone reductase reaction catalyzed by submitochondrial particles. Biochim Biophys Acta. 1998 May 6;1364(2):287-96. Mitochondrial NADH:ubiquinone-reductase (Complex I) catalyzes translocation into inside-out submitochondrial particles. Thus, thermally induced deactivation of Complex I as well as specific inhibitors of the endogenous reduction (rotenone, piericidin A) do not inhibit the translocating activity of the enzyme. |
2(0,0,0,2) | Details |
2721632 | Davies KP, Zahner H, Kohler P: Litomosoides carinii: mode of action in vitro of benzothiazole and amoscanate derivatives with antifilarial activity. Exp Parasitol. 1989 May;68(4):382-91. It was confirmed that the drugs CGP 20376, 21835, 20308, 21306, and 6140 cause a rapid immobilization in vitro of the adult filarial worm, Litomosoides carinii, the time required being similar to rotenone at the same concentration. This effect on SMP respiration could be overcome by using as a substrate, indicating the site of inhibition to be within complex I of the mitochondrial respiratory chain. |
2(0,0,0,2) | Details |
19486265 | Hajieva P, Mocko JB, Moosmann B, Behl C: Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity. J Neurochem. 2009 Jul;110(1):118-32. Epub 2009 May 26. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or depletion. We have found that exceptionally low concentrations (EC (50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP (+), rotenone, and l-buthionine sulfoximine. |
1(0,0,0,1) | Details |
12842875 | Lee JM, Shih AY, Murphy TH, Johnson JA: NF-E2-related factor-2 mediates neuroprotection against mitochondrial complex I inhibitors and increased concentrations of intracellular in primary cortical neurons. Int J Parasitol. 1995 Jan;25(1):15-21. Nrf2-/- neurons in this mixed culture system were more sensitive to mitochondrial toxin (1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine or rotenone)-induced apoptosis compared with Nrf2+/+ neurons. |
1(0,0,0,1) | Details |
18615648 | Schuh RA, Matthews CC, Fishman PS: Interaction of mitochondrial respiratory inhibitors and excitotoxins potentiates cell death in hippocampal slice cultures. J Neurosci Res. 2008 Nov 15;86(15):3306-13. The broad-spectrum insecticide rotenone, an inhibitor of complex I of the mitochondrial electron transport chain (ETC), gives rise to oxidative stress and bioenergetic failure. The broad-spectrum insecticide rotenone, an inhibitor of complex I of the mitochondrial electron transport chain (ETC), gives rise to oxidative stress and bioenergetic failure. |
1(0,0,0,1) | Details |
8806593 | Guidarelli A, Brambilla L, Cattabeni F, Cantoni O: Rotenone, an inhibitor of complex I, abolished both effects but did not, however, affect the DNA SSB-frequency observed after treatment with tB-OOH alone. Rotenone, an inhibitor of complex I, abolished both effects but did not, however, affect the DNA SSB-frequency observed after treatment with tB-OOH alone. |
enhances DNA single-strand break formation while abolishing cytotoxicity in U937 cells exposed to tert-butylhydroperoxide. J Neurochem. 2007 Oct;103(1):131-44.1(0,0,0,1) | Details |
7666176 | Marey-Semper I, Gelman M, Levi-Strauss M: A selective toxicity toward cultured mesencephalic dopaminergic neurons is induced by the synergistic effects of energetic metabolism impairment and NMDA receptor activation. Biochem Pharmacol. 2003 Jan 1;65(1):51-7. In order to demonstrate the existence of such a selective vulnerability, the toxic effects of rotenone, an inhibitor of complex I of the respiratory chain, and of which is very likely involved in the neurotoxicity induced by an energetic stress, were analyzed on cultured mouse mesencephalic neurons. In order to demonstrate the existence of such a selective vulnerability, the toxic effects of rotenone, an inhibitor of complex I of the respiratory chain, and of which is very likely involved in the neurotoxicity induced by an energetic stress, were analyzed on cultured mouse mesencephalic neurons. |
1(0,0,0,1) | Details |
16979221 | Leiser SF, Salmon AB, Miller RA: Correlated resistance to fibroblast cell lines from long-lived pituitary dwarf mice. Planta. 2001 Apr;212(5-6):765-73. Snell dwarf fibroblasts are here reported to differ from control cell lines in two other respects: they are relatively resistant to the metabolic inhibition induced by low concentrations, and also resistant to the effects of the mitochondrial poison rotenone, a blocker of Complex I of the electron transport chain. Snell dwarf fibroblasts are here reported to differ from control cell lines in two other respects: they are relatively resistant to the metabolic inhibition induced by low concentrations, and also resistant to the effects of the mitochondrial poison rotenone, a blocker of Complex I of the electron transport chain. |
deprivation and cytotoxic agents in 1(0,0,0,1) | Details |
15560892 | Belyaeva EA, Glazunov VV, Korotkov SM: Cd2+ versus Ca2+-produced mitochondrial membrane permeabilization: a proposed direct participation of respiratory complexes I and III. Mech Ageing Dev. 2006 Nov;127(11):821-9. Epub 2006 Sep 18. A possible involvement of respiratory chain components, namely complex I (P-site) and complex III (S-site) in Cd2+ and/or Ca2+-produced MMP was discussed. Similarity and distinction in action of rotenone, oligomycin, N-ethylmaleimide, catalase, dibucaine, ruthenium red, cyclosporin A (CsA), and ADP on Cd2+ and/or Ca2+-induced mitochondrial dysfunction were revealed. |
1(0,0,0,1) | Details |
15934940 | Moon Y, Lee KH, Park JH, Geum D, Kim K: Mitochondrial membrane depolarization and the selective death of dopaminergic neurons by rotenone: protective effect of Biochem J. 1997 Dec 15;328 ( Pt 3):801-6. This action is thought to be relevant to its inhibition of the mitochondrial complex I, but the precise mechanism of this suppression in selective neuronal death is still elusive. |
1(0,0,0,1) | Details |
16531806 | Lijnen P, Papparella I, Petrov V, Semplicini A, Fagard R: Angiotensin II-stimulated collagen production in cardiac fibroblasts is mediated by reactive species. Biochemistry. 1992 Nov 24;31(46):11425-34. CONCLUSIONS: Our data show that in adult rat cardiac fibroblasts the membrane-associated NAD (P) H oxidase complex is the predominant source of and reactive species generation in angiotensin II-stimulated adult cardiac fibroblasts. Rotenone, allopurinol, indomethacin, nordihydroguiaretic acid, ketoconazole and nitro- (inhibitors of mitochondrial NAD (P) H oxidase, xanthine oxidase, cyclooxygenase, lipoxygenase, cytochrome P450 oxygenase and synthase, respectively) did not affect the angiotensin II-induced collagen production. |
1(0,0,0,1) | Details |
20151456 | Lohrke B, Xu J, Weitzel JM, Kruger B, Goldammer T, Viergutz T: A protonophore restored Deltapsi and rotenone (an inhibitor of respiratory chain complex I) inhibited mitochondrial recovering. A protonophore restored Deltapsi and rotenone (an inhibitor of respiratory chain complex I) inhibited mitochondrial recovering. |
impairs survival of luteal cells through mitochondrial dysfunction. J Bioenerg Biomembr. 2000 Dec;32(6):609-15.1(0,0,0,1) | Details |
15698934 | Wang XJ, Xu JX: Possible involvement of Ca2+ signaling in rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells. J Neurochem. 2003 Jul;86(1):196-209. Rotenone, an inhibitor of mitochondrial respiratory chain complex I, is a useful tool to elicit animal model of Parkinson's disease. |
1(0,0,0,1) | Details |
7622333 | Armson A, Grubb WB, Mendis AH: Strongyloides ratti: mitochondrial enzyme activities of the classical electron transport pathway in the infective (L3) larvae. Neurotox Res. 2006 Jan;9(1):47-57. The NCR and NOX activities were 39.3% and 23.5% of the NFR activity, suggesting the occurrence of a rate-limiting step or bifurcation of the respiratory electron transport (RET) pathway on the -side of RET-Complex I. Antimycin A and rotenone but not 2-thenoyl trifluoroacetone (TTFA) inhibited NCR activity, the EC50 values were 3.6 x 10 (-6) M, 3.7 x 10 (-7) M, respectively. |
1(0,0,0,1) | Details |
11097871 | Gennari A, Viviani B, Galli CL, Marinovich M, Pieters R, Corsini E: Organotins induce apoptosis by disturbance of [Ca (2+)](i) and mitochondrial activity, causing oxidative stress and activation of caspases in rat thymocytes. Blood. 2005 Feb 15;105(4):1717-23. Epub 2004 Oct 14. ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular Ca (2+) chelator, or rotenone, an inhibitor of the electron entry from complex I to indicating the important role of Ca (2+) and mitochondria during these early intracellular events. ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular Ca (2+) chelator, or rotenone, an inhibitor of the electron entry from complex I to indicating the important role of Ca (2+) and mitochondria during these early intracellular events. |
1(0,0,0,1) | Details |
2827635 | Reed JS, Ragan CI: The effect of rate limitation by cytochrome c on the redox state of the pool in reconstituted cytochrome c reductase. J Cardiovasc Pharmacol. 2008 May;51(5):483-91. These conditions can be met by reconstituted cytochrome c reductase (Complex I-III from bovine heart) when electron flow is rate-limited by a low concentration of cytochrome c. We show that, in such a system, the dependence of activity (varied by inhibition with rotenone) on the steady-state level of reduction is indeed non-linear and very closely accounted for by the theory. |
1(0,0,0,1) | Details |
19120153 | Moldzio R, Piskernik C, Radad K, Rausch WD: Rotenone damages striatal organotypic slice culture. Clin Exp Pharmacol Physiol. 2009 Oct;36(10):e57-64. Epub 2009 Jun 8. Exposure to rotenone results in degeneration of the nigrostriatal pathway through inhibition of complex I. |
81(1,1,1,1) | Details |
16952382 | Panesar NS, Chan KW: Evidence for tumor cells. Free Radic Biol Med. 2008 May 1;44(9):1762-71. Epub 2008 Feb 13. In stimulated MLTC-1, MRCC inhibitors decreased production, order being: complex III (antimycin A and myxothiazol) > complex I (rotenone) > complex II (thenoyltrifluoroacetone), while cAMP production increased inversely. |
reductase activity in intact mouse Leydig 81(1,1,1,1) | Details |
9350628 | Mojet MH, Mills E, Duchen MR: Hypoxia-induced catecholamine secretion in isolated newborn rat chromaffin cells is mimicked by inhibition of mitochondrial respiration. BMC Neurosci. 2007 Aug 16;8:67. Inhibition of mitochondrial respiration either by CN- at complex IV or by rotenone at complex I mimicked severe hypoxia, reversibly increasing both [Ca2+] i and catecholamine secretion. |
81(1,1,1,1) | Details |
16034640 | Baby SM, Roy A, Lahiri S: Role of mitochondria in the regulation of hypoxia-inducible factor-1alpha in the rat carotid body glomus cells. Methods Enzymol. 2009;456:169-81. To test this hypothesis in the CB glomus cells, we studied the effect of mitochondrial electron transport chain (ETC) inhibitors: rotenone (complex I; 1 microM), (complex II; 0.5 M), antimycin A (complex III; 1 microg/ml), azide (complex IV; 5 mM), and uncoupler of oxidative phosphorylation: carbonyl p-trifluoromethoxyphenylhydrazone (FCCP; 1 mM) on HIF-1alpha expression during normoxia and hypoxia. |
81(1,1,1,1) | Details |
12151787 | Lehmensiek V, Tan EM, Schwarz J, Storch A: Expression of mutant alpha-synucleins enhances dopamine transporter-mediated MPP+ toxicity in vitro. J Bioenerg Biomembr. 2002 Dec;34(6):413-21. We demonstrate that expression of all alpha-synuclein isoforms enhances toxicity of general complex I inhibition (rotenone), but only the expression of mutant alpha-synucleins induces significant increased DAT-dependent toxicity of very low concentrations of MPP+ compared to wild-type protein. |
81(1,1,1,1) | Details |
11181577 | Petruzzella V, Vergari R, Puzziferri I, Boffoli D, Lamantea E, Zeviani M, Papa S: A nonsense mutation in the NDUFS4 gene encoding the 18 kDa (AQDQ) subunit of complex I abolishes assembly and activity of the complex in a patient with Leigh-like syndrome. J Biol Chem. 2001 Nov 2;276(44):41394-8. Epub 2001 Aug 29. Fibroblast cultures from the patient exhibited severe reduction of the rotenone-sensitive --> UQ oxidoreductase activity of complex I, which was insensitive to cAMP stimulation. |
35(0,1,1,5) | Details |
9452319 | Blandini F, Nappi G, Greenamyre JT: Quantitative study of mitochondrial complex I in platelets of parkinsonian patients. Life Sci. 2009 Aug 12;85(7-8):276-80. Epub 2009 Jun 9. To obtain quantitative information on platelet complex I in PD, we studied platelet complex I in 16 PD patients and 16 age-matched controls by using a newly developed technique based on the binding of [3H] dihydrorotenone ([3H] DHR), an analog of the pesticide rotenone, to complex I. |
35(0,1,1,5) | Details |
14521988 | Lannuzel A, Michel PP, Hoglinger GU, Champy P, Jousset A, Medja F, Lombes A, Darios F, Gleye C, Laurens A, Hocquemiller R, Hirsch EC, Ruberg M: The mitochondrial complex I inhibitor annonacin is toxic to mesencephalic dopaminergic neurons by impairment of energy metabolism. IUBMB Life. 2004 Aug;56(8):477-82. The death of dopaminergic neurons induced by systemic administration of mitochondrial respiratory chain complex I inhibitors such as 1-methyl-4-phenylpyridinium (MPP (+); given as the prodrug 1-methyl-1,2,3,6-tetrahydropyridine) or the pesticide rotenone have raised the question as to whether this family of compounds are the cause of some forms of Parkinsonism. |
33(0,1,1,3) | Details |
8512593 | Anderson WM, Wood JM, Anderson AC: Inhibition of mitochondrial and Paracoccus denitrificans -ubiquinone reductase by oxacarbocyanine dyes. Toxicol Appl Pharmacol. 2009 Oct 15;240(2):198-207. Epub 2009 Jul 17. The mechanism of inhibition of the oxacarbocyanines appears to be similar to that of rotenone since (a) essentially only electron acceptors affected by rotenone were affected by the compounds, (b) inhibition of reduction was diminished drastically with rotenone-saturated SMP, and (c) inhibition of was largely eliminated with rotenone-insensitive complex I, and P. denitrificans membrane vesicles. |
33(0,1,1,3) | Details |
18492763 | Koppers AJ, De Iuliis GN, Finnie JM, McLaughlin EA, Aitken RJ: Significance of mitochondrial reactive spermatozoa. Int J Biol Sci. 2007 Jul 13;3(5):335-41. RESULTS: Disruption of mitochondrial electron transport flow in human spermatozoa resulted in generation of ROS from complex I (rotenone sensitive) or III (myxothiazol, antimycin A sensitive) via mechanisms that were independent of mitochondrial membrane potential. |
species in the generation of oxidative stress in 32(0,1,1,2) | Details |
18687689 | Selivanov VA, Zeak JA, Roca J, Cascante M, Trucco M, Votyakova TV: The role of external and matrix pH in mitochondrial reactive ROS production increase induced by the alkalization of medium was observed with intact respiring mitochondria as well as in the presence of complex I inhibitor rotenone, which enhanced reactive species release. |
species generation. J Bioenerg Biomembr. 2008 Dec;40(6):587-98. Epub 2008 Nov 14.32(0,1,1,2) | Details |
10486562 | Hohler B, Lange B, Holzapfel B, Goldenberg A, Hanze J, Sell A, Testan H, Moller W, Kummer W: Hypoxic upregulation of tyrosine hydroxylase gene expression is paralleled, but not induced, by increased generation of reactive species in PC12 cells. FEBS Lett. 1999 Aug 20;457(1):53-6. This increase is abolished by intracellular scavenging by Mn (III)-tetrakis (1-methyl-4-pyridyl)- and reduced or absent in the presence of the flavoprotein/complex I inhibitors, diphenyl-eneiodonium and rotenone. |
31(0,1,1,1) | Details |
18854758 | Nozoe M, Hirooka Y, Koga Y, Araki S, Konno S, Kishi T, Ide T, Sunagawa K: Mitochondria-derived reactive species mediate sympathoexcitation induced by angiotensin II in the rostral ventrolateral medulla. J Hypertens. 2008 Nov;26(11):2176-84. Overexpression of Mn-SOD and rotenone, a mitochondrial respiratory complex I inhibitor, suppressed AngII-induced ROS production. |
31(0,1,1,1) | Details |
12358746 | Starkov AA, Polster BM, Fiskum G: Regulation of production by brain mitochondria by and Bax. Plant Physiol Biochem. 2005 Jan;43(1):61-7. In the presence of the respiratory chain Complex I inhibitor rotenone, accumulation of Ca2+ stimulated H2O2 production by mitochondria oxidizing and this stimulation was associated with release of mitochondrial cytochrome c. |
peroxide 31(0,1,1,1) | Details |
18801963 | Garciarena CD, Caldiz CI, Correa MV, Schinella GR, Mosca SM, Chiappe de Cingolani GE, Cingolani HE, Ennis IL: Na+/H+ exchanger-1 inhibitors decrease myocardial production via direct mitochondrial action. Mol Aspects Med. 1997;18 Suppl:S263-7. The mitochondria appeared to be the source of the NOX-dependent ROS released by the "ROS-induced ROS release mechanism" that was blunted by the mitochondrial ATP-sensitive potassium channel blockers 5-hydroxydecanoate and glibenclamide, inhibition of complex I of the electron transport chain with rotenone, and inhibition of the permeability transition pore (MPTP) by cyclosporin A. |
31(0,1,1,1) | Details |
16239214 | Ved R, Saha S, Westlund B, Perier C, Burnam L, Sluder A, Hoener M, Rodrigues CM, Alfonso A, Steer C, Liu L, Przedborski S, Wolozin B: Similar patterns of mitochondrial vulnerability and rescue induced by genetic modification of alpha-synuclein, parkin, and DJ-1 in Caenorhabditis elegans. Int J Parasitol. 1995 Feb;25(2):257-60. C. elegans lines with these genetic changes were more vulnerable than nontransgenic nematodes to mitochondrial complex I inhibitors, including rotenone, fenperoximate, pyridaben, or stigmatellin. |
31(0,1,1,1) | Details |
1664494 | Benzi G, Curti D, Pastoris O, Marzatico F, Villa RF, Dagani F: Sequential damage in mitochondrial complexes by peroxidative stress. Neurosci Lett. 2005 Mar 11;376(2):127-32. Epub 2004 Dec 9. The cerebral peroxidative stress induces: (a) initially, a decrease in brain GSH concentration concomitant with a decrease in the mitochondrial activity of cytochrome oxidase of aa3-type (complex IV), without changes in and cytochrome b populations; (b) subsequently, an alteration in the transfer molecule cytochrome c and, finally, in rotenone-sensitive -cytochrome c reductase (complex I) and succinate dehydrogenase (complex II). |
31(0,1,1,1) | Details |
15486067 | Kim JH, Chu SC, Gramlich JL, Pride YB, Babendreier E, Chauhan D, Salgia R, Podar K, Griffin JD, Sattler M: Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive species. Neurochem Res. 1991 Dec;16(12):1295-302. Elevated ROS levels in BCR-ABL-transformed cells were found to be blocked by the mitochondrial complex I inhibitor rotenone as well as the transport inhibitor suggesting that the source of increased ROS might be related to increased metabolism. |
31(0,1,1,1) | Details |
10220277 | Konishi K, Tanaka T: Inhibitory effects of tannins on the NADH dehydrogenase activity of bovine heart mitochondrial complex I. Toxicol Appl Pharmacol. 2001 Sep 1;175(2):160-8. - oxidoreductase activity of complex I was susceptible to the three tannins, but completely resistant to rotenone. |
10(0,0,1,5) | Details |
16963630 | Cardol P, Lapaille M, Minet P, Franck F, Matagne RF, Remacle C: ND3 and ND4L subunits of mitochondrial complex I, both nucleus encoded in Chlamydomonas reinhardtii, are required for activity and assembly of the enzyme. Ann Neurol. 1999 Oct;46(4):587-97. Made of more than 40 subunits, the rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) is the most intricate membrane-bound enzyme of the mitochondrial respiratory chain. |
10(0,0,1,5) | Details |
20224768 | Sarafian TA, Montes C, Imura T, Qi J, Coppola G, Geschwind DH, Sofroniew MV: Disruption of astrocyte STAT3 signaling decreases mitochondrial function and increases oxidative stress in vitro. J Exp Biol. 2003 Feb;206(Pt 4):651-8. Many of the differences observed in STAT3-CKO astrocytes were distinctly altered by exposure to rotenone, suggesting a role for complex I of the mitochondrial electron transport chain. |
6(0,0,1,1) | Details |
1629744 | Greenamyre JT, Higgins DS, Eller RV: Quantitative autoradiography of dihydrorotenone binding to complex I of the electron transport chain. Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2614-21. Epub 2006 Oct 5. Unlabeled rotenone and 1-methyl-4-phenylpyridinium ion competed effectively for DHR binding sites. |
5(0,0,0,5) | Details |
11418099 | Schuler F, Casida JE: Functional coupling of PSST and ND1 subunits in NADH:ubiquinone oxidoreductase established by photoaffinity labeling. J Biol Chem. 1975 Nov 10;250(21):8472-6. NADH:ubiquinone oxidoreductase (complex I) is the first, largest and most complicated enzyme of the mitochondrial electron transport chain. |
5(0,0,0,5) | Details |
18763029 | Zoccarato F, Cappellotto M, Alexandre A: Clorgyline and other propargylamine derivatives as inhibitors of -dependent H (2) O (2) release at NADH:UBIQUINONE oxidoreductase (Complex I) in brain mitochondria. Bioorg Med Chem Lett. 2003 Nov 17;13(22):4101-5. O (2)(-) release is low with NAD-linked substrates and increases strongly during oxidation, which increases the QH (2)/Q ratio and is rotenone sensitive. |
3(0,0,0,3) | Details |
1445878 | Heinrich H, Werner S: Identification of the binding site of NADH:ubiquinone oxidoreductase (complex I) from Neurospora crassa. J Neurochem. 2009 Feb;108(4):1045-56. The activity of the enzyme applying these derivatives is inhibited by 50% at a concentration of 9 and 20 microM rotenone. |
-3(0,0,0,3) | Details |
8619621 | Schonheit K, Nohl H: Oxidation of cytosolic via complex I of heart mitochondria. . Arch Biochem Biophys. 1996 Mar 15;327(2):319-23. Our studies exclude both the rotenone-insensitive NADH dehydrogenase of the outer membrane and the endogenous NADH dehydrogenase of damaged mitochondria as being responsible for external consumption. |
2(0,0,0,2) | Details |
17521330 | Cermakova P, Verner Z, Man P, Lukes J, Horvath A: Characterization of the NADH:ubiquinone oxidoreductase (complex I) in the trypanosomatid Phytomonas serpens (Kinetoplastida). Biochem Biophys Res Commun. 1996 Sep 4;226(1):70-4. Spectrophotometric measurement of the NADH:ubiquinone 10 and NADH:ferricyanide dehydrogenase activities revealed their different sensitivities to rotenone, piericidin, and diphenyl iodonium. |
2(0,0,0,2) | Details |
18427623 | Levin LA: Mechanisms of retinal ganglion specific-cell death in Leber hereditary optic neuropathy. Neurotox Res. 2008 Dec;14(4):367-82. RESULTS: The rate of production in brain mitochondria was more than 5 times the rate in RGC-5 cells when complex I substrates were used. Rotenone significantly increased the rate of production in brain but not RGC-5 mitochondria. |
1(0,0,0,1) | Details |
6786284 | Takeshige K, Takayanagi R, Minakami S: Lipid peroxidation and the reduction of ADP-Fe3+ chelate by -ubiquinone reductase preparation from bovine heart mitochondria. Biochem J. 1980 Dec 15;192(3):861-6. The -ubiquinone reductase preparation (Complex I) of bovine hart mitochondria catalysed in the presence of reduced coenzymes and ADP-Fe3+ the lipid peroxidation of liposomes prepared from mitochondrial lipids. The apparent Km values for the coenzymes and the optimal pH of the reactions agreed well with those of the lipid peroxidation of the submitochondrial particles treated with rotenone. |
1(0,0,0,1) | Details |
16543632 | Itoh Y, Takaoka R, Ohira M, Abe T, Tanahashi N, Suzuki N: Reactive brain microvessel endothelial cells. Clin Hemorheol Microcirc. 2006;34(1-2):163-8. Injury to mitochondrial respiratory chain was induced either with rotenone (an inhibitor of mitochondrial complex I) or with m-chlorocarbonyl phenylhydrazone (CCCP) (an uncoupler of ATP synthetase). Injury to mitochondrial respiratory chain was induced either with rotenone (an inhibitor of mitochondrial complex I) or with m-chlorocarbonyl phenylhydrazone (CCCP) (an uncoupler of ATP synthetase). |
species generated by mitochondrial injury in human 1(0,0,0,1) | Details |
19515065 | Dong L, Xie MJ, Zhang P, Ji LL, Liu WC, Dong MQ, Gao F: Rotenone partially reverses decreased BK Ca currents in cerebral artery smooth muscle cells from streptozotocin-induced diabetic mice. Biochim Biophys Acta. 2001 Jul 2;1506(1):79-87. Control and diabetic mice were treated with 12.7 micromol/L rotenone, an inhibitor of the mitochondrial electron transport chain complex I, or placebo every other day for 5 weeks. |
1(0,0,0,1) | Details |
9878636 | Duby F, Matagne RF: Alteration of dark respiration and reduction of phototrophic growth in a mitochondrial DNA deletion mutant of Chlamydomonas lacking cob, nd4, and the 3' end of nd5. Hum Mol Genet. 2001 Mar 1;10(5):529-35. Due to these mitochondrial DNA alterations, complex I activity, the cytochrome pathway of respiration, and presumably, the three phosphorylation sites associated with these enzyme activities are lacking in the mutant. The low respiratory rate of the dum24 cells results from the activities of rotenone-resistant NADH dehydrogenase, complex II, and alternative oxidase, with none of these enzymes being coupled to ATP production. |
1(0,0,0,1) | Details |
16624679 | Rizzardini M, Lupi M, Mangolini A, Babetto E, Ubezio P, Cantoni L: Neurodegeneration induced by complex I inhibition in a cellular model of familial amyotrophic lateral sclerosis. Plant Cell. 1999 Jan;11(1):115-25. G93A Cu/Zn superoxide dismutase (SOD1), a human mutant SOD1 associated with familial amyotrophic lateral sclerosis, increased the toxicity of the mitochondrial toxin rotenone in the NSC-34 motoneuronal cell line. |
1(0,0,0,1) | Details |
14592541 | Tudella VG, Curti C, Soriani FM, Santos AC, Uyemura SA: In situ evidence of an alternative oxidase and an uncoupling protein in the respiratory chain of Aspergillus fumigatus. Mov Disord. 1998 Jan;13(1):11-5. Firstly, a functional respiratory chain (complex I-V) was demonstrated: (ADP) induced an oligomycin-sensitive transition from resting to phophorylating respiration in the presence of the oxidizable substrates alpha-ketoglutarate, dihydroorotate, N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD) and exogenous In addition, the ability of the fungus to oxidize exogenous as well as the insensitivity of its respiration to rotenone, in association with the sensitivity to indicate the presence of an alternative NADH-ubiquinone oxidoreductase; the partial sensitivity of respiration to antimycin A and in association with the sensitivity to benzohydroxamic acid, indicates the presence of an alternative oxidase. |
1(0,0,0,1) | Details |
9603924 | Barrientos A, Kenyon L, Moraes CT: Human xenomitochondrial cybrids. J Biol Chem. 2009 Jan 23;284(4):2045-52. Epub 2008 Dec 1. Kinetic studies of complex I using decylubiquinone or as limiting substrates showed that the Vmax was decreased in HXC by approximately 40%, and the Km for the was significantly increased (3-fold, p < 0.001). Rotenone inhibition studies of intact cell respiration and - oxidation in permeabilized cells showed that 3 nM rotenone produced a mild effect in control cells (0-10% inhibition) but produced a marked inhibition of HXC respiration (50-75%). |
1(0,0,0,1) | Details |
12176058 | Young TA, Cunningham CC, Bailey SM: Reactive production by the mitochondrial respiratory chain in isolated rat hepatocytes and liver mitochondria: studies using myxothiazol. Neuroscience. 2010 Jan 20;165(2):455-62. Epub . Coincubation with antimycin or rotenone had no effect on myxothiazol-induced ROS levels. Furthermore, diphenyliodonium, an inhibitor that blocks electron flow through the of mitochondrial complex I and other flavoenzymes, significantly attenuated the myxothiazol-induced increase in hepatocyte ROS levels. |
species 1(0,0,0,1) | Details |
12853461 | Pelicano H, Feng L, Zhou Y, Carew JS, Hileman EO, Plunkett W, Keating MJ, Huang P: Inhibition of mitochondrial respiration: a novel strategy to enhance drug-induced apoptosis in human leukemia cells by a reactive species-mediated mechanism. PLoS One. 2009;4(1):e4160. Epub 2009 Jan 8. This strategy was first tested in a proof-of-principle study using rotenone, a specific inhibitor of mitochondrial electron transport complex I. |
81(1,1,1,1) | Details |
18599602 | Watabe M, Nakaki T: Mitochondrial complex I inhibitor rotenone inhibits and redistributes vesicular monoamine transporter 2 via nitration in human dopaminergic SH-SY5Y cells. Mol Pharmacol. 2008 Oct;74(4):933-40. Epub 2008 Jul 3. Long-term systemic mitochondrial complex I inhibition by rotenone induces selective degeneration of dopaminergic neurons in rats. |
81(1,1,1,1) | Details |
10841308 | de Halac IN, Bacman SR, de Kremer RD: Histoenzymology of oxidases and dehydrogenases in peripheral blood lymphocytes and monocytes for the study of mitochondrial oxidative phosphorylation. Toxicol Sci. 2007 Jan;95(1):196-204. Epub 2006 Oct 12. Complex I activity was detected, but inhibition with rotenone was incomplete. |
81(1,1,1,1) | Details |
15924876 | Li J, French BA, Nan L, Fu P, French SW: Uncoupling of oxidative phosphorylation prevents the urinary The question was: is the rate of oxidative phosphorylation fluxuation essential for the cycle to occur? The question has been partially answered by showing that rotenone, which inhibits complex I, blocks the cycle by preventing the generation of NAD from |
level cycling caused by feeding continuously at a constant rate. Anal Biochem. 2003 Feb 1;313(1):46-52.81(1,1,1,1) | Details |
1445939 | Kotlyar AB, Gutman M: The effect of delta mu H+ on the interaction of rotenone with complex I of submitochondrial particles. Mol Pharmacol. 1998 Jun;53(6):1076-82. |
81(1,1,1,1) | Details |
16412576 | Chen MJ, Yap YW, Choy MS, Koh CH, Seet SJ, Duan W, Whiteman M, Cheung NS: Early induction of calpains in rotenone-mediated neuronal apoptosis. Biochim Biophys Acta. 1992 Dec 7;1140(2):169-74. Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson's disease (PD), where neurons undergo apoptosis by caspase-dependent and/or caspase-independent pathways. |
81(1,1,1,1) | Details |
10982813 | Seo BB, Wang J, Flotte TR, Yagi T, Matsuno-Yagi A: Use of the quinone oxidoreductase (NDI1) gene of Saccharomyces cerevisiae as a possible cure for complex I defects in human cells. Brain Res Bull. 2006 Apr 28;69(4):465-74. Epub 2006 Mar 10. Furthermore, when cells were cultured under the conditions where energy has to be provided by respiration, the NDI1-transduced cells were able to grow even in the presence of added complex I inhibitor such as rotenone and 1-methyl-4-phenylpyridinium ion. |
-35(0,1,1,5) | Details |
16581014 | Yagi T, Seo BB, Nakamaru-Ogiso E, Marella M, Barber-Singh J, Yamashita T, Matsuno-Yagi A: Possibility of transkingdom gene therapy for complex I diseases. Brain Res Bull. 2007 Mar 30;71(6):633-40. Epub 2007 Jan 8. The NDI1-transduced cells were more resistant to complex I inhibitors and diminished production of reactive species induced by rotenone. |
35(0,1,1,5) | Details |
15228597 | Gyulkhandanyan AV, Pennefather PS: Shift in the localization of sites of production in brain mitochondria by mitochondrial stress. Arterioscler Thromb Vasc Biol. 2005 Jul;25(7):1401-7. Epub 2005 Apr 21. H (2) O (2) production supported by during reverse transfer of electrons was decreased by inhibitors of complex I (rotenone and diphenyleneiodonium) whereas in / -oxidizing mitochondria diphenyleneiodonium decreased while rotenone increased H (2) O (2) generation. |
peroxide 33(0,1,1,3) | Details |
9989245 | Cassarino DS, Parks JK, Parker WD Jr, Bennett JP Jr: The parkinsonian neurotoxin MPP+ opens the mitochondrial permeability transition pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism. Biol Pharm Bull. 2003 May;26(5):729-32. Rotenone, a classic non-competitive complex I inhibitor, completely inhibited MPP (+)-induced swelling and release of cytochrome c. |
33(0,1,1,3) | Details |
17292807 | Kim YJ, Ko HH, Han ES, Lee CS: inhibition of rotenone- or 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death. J Neurosci Res. 2004 May 15;76(4):563-71. The aim of the present study was to assess the effect of antiepileptic against the cytotoxicity of mitochondrial respiratory complex I inhibitors rotenone and 1-methyl-4-phenylpyridinium (MPP+) in relation to the mitochondria-mediated cell death process and oxidative stress. |
32(0,1,1,2) | Details |
15540952 | Caboni P, Sherer TB, Zhang N, Taylor G, Na HM, Greenamyre JT, Casida JE: Rotenone, deguelin, their metabolites, and the rat model of Parkinson's disease. J Immunol. 2006 Jul 15;177(2):852-62. We previously established that the hydroxylated metabolites and derivatives of rotenone and deguelin are all less active (i.e., detoxified) as complex I inhibitors relative to the parent rotenoids. |
32(0,1,1,2) | Details |
14505934 | Deng Y, Nicholson RA: Stimulation by surangin B of endogenous amino acid release from synaptosomes. Basic Clin Pharmacol Toxicol. 2010 Jan;106(1):53-61. Epub 2009 Oct 28. Rotenone (a complex I inhibitor) and carbonyl chlorophenylhydrazone (CCCP; an uncoupler), were more potent releasers of amino acids from synaptosomes than surangin B, however, carboxin (a complex II-selective inhibitor), was extremely weak to ineffective in this regard. |
32(0,1,1,2) | Details |
19885011 | Kim HJ, Song JY, Park HJ, Park HK, Yun DH, Chung JH: Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells. Korean J Physiol Pharmacol. 2009 Aug;13(4):281-5. Epub 2009 Aug 31. Rotenone, a mitochondrial complex I inhibitor, can induce the pathological features of Parkinson's disease (PD). |
Protects against 31(0,1,1,1) | Details |
19741132 | Ng CH, Mok SZ, Koh C, Ouyang X, Fivaz ML, Tan EK, Dawson VL, Dawson TM, Yu F, Lim KL: Parkin protects against LRRK2 G2019S mutant-induced dopaminergic neurodegeneration in Drosophila. J Biol Chem. 2002 Nov 22;277(47):44784-90. Epub 2002 Sep 16. Furthermore, LRRK2 mutant flies also display reduced lifespan and increased sensitivity to rotenone, a mitochondrial complex I inhibitor. |
31(0,1,1,1) | Details |
15910763 | Grammatopoulos TN, Ahmadi F, Jones SM, Fariss MW, Weyhenmeyer JA, Zawada WM: Angiotensin II protects cultured midbrain dopaminergic neurons against rotenone-induced cell death. Brain Res. 2005 May 31;1045(1-2):64-71. Epub 2005 Apr 26. Primary ventral mesencephalic (VM) cultures from E15 rats were grown for 5 days and then cultured in the presence of the mitochondrial complex I inhibitor, rotenone. |
31(0,1,1,1) | Details |
16378625 | Wu CC, Hsu MC, Hsieh CW, Lin JB, Lai PH, Wung BS: Upregulation of heme oxygenase-1 by via the phosphatidylinositol 3-kinase/Akt and ERK pathways. J Bioenerg Biomembr. 2002 Jun;34(3):193-208. The inhibition of intracellular ROS production by (NAC), (GSH), superoxide dismutase (SOD), catalase and the mitochondrial complex I inhibitor, rotenone, results in a decrease in -dependent HO-1 expression. |
31(0,1,1,1) | Details |
18353897 | Koopman WJ, Distelmaier F, Hink MA, Verkaart S, Wijers M, Fransen J, Smeitink JA, Willems PH: Inherited complex I deficiency is associated with faster protein diffusion in the matrix of moving mitochondria. J Biol Chem. 1988 Nov 25;263(33):17566-75. We demonstrated previously that inhibition of mitochondrial complex I (CI or NADH:ubiquinone oxidoreductase) by rotenone accelerated matrix protein diffusion and decreased the fraction and velocity of moving mitochondria. |
31(0,1,1,1) | Details |
15545227 | Scatena R, Martorana GE, Bottoni P, Giardina B: Mitochondrial dysfunction by synthetic ligands of peroxisome proliferator activated receptors (PPARs). Exp Toxicol Pathol. 1993 Oct;45(5-6):375-80. A re-evaluation of the biological activities of PPAR synthetic ligands, in particular of the mitochondrial dysfunction based on a rotenone-like Complex I partial inhibition and of its consequent metabolic adaptations, seems to explain some of the pathophysiologic aspects of PPARs allowing a better definition of the therapeutic properties of the so-called PPAR-ligands. |
31(0,1,1,1) | Details |
19857556 | Li X, Liu Z, Tamashiro K, Shi B, Rudnicki DD, Ross CA, Moran TH, Smith WW: Synphilin-1 exhibits trophic and protective effects against Rotenone toxicity. Toxicol Appl Pharmacol. 2000 Dec 1;169(2):185-90. Rotenone, mitochondrial complex I inhibitor, has been shown previously to induce dopaminergic neurodegeneration and Parkinsonism in rats and Drosophila. |
31(0,1,1,1) | Details |
19409896 | Greene JG, Noorian AR, Srinivasan S: Delayed gastric emptying and enteric nervous system dysfunction in the rotenone model of Parkinson's disease. Arch Biochem Biophys. 2002 Sep 1;405(1):65-72. We report that the parkinsonian neurotoxin and mitochondrial complex I inhibitor rotenone causes delayed gastric emptying and enteric neuronal dysfunction when administered chronically to rats in the absence of major motor dysfunction or CNS pathology. |
31(0,1,1,1) | Details |
7632092 | Campos Y, Arenas J, Cabello A, Gomez-Reino JJ: Respiratory chain enzyme defects in patients with idiopathic inflammatory myopathy. Stem Cells. 2008 Jan;26(1):64-71. Epub 2007 Oct 18. Activity of rotenone sensitive cytochrome c reductase (complex I and III) succinate dehydrogenase (complex II), cytochrome c reductase (complex II and III), cytochrome c oxidase (complex IV), and citrate synthase (a mitochondrial matrix enzyme), was measured spectrophotometrically in muscle homogenates. |
31(0,1,1,1) | Details |
19854245 | Brawek B, Loffler M, Wagner K, Huppertz HJ, Wendling AS, Weyerbrock A, Jackisch R, Feuerstein TJ: Reactive The increase in the concentration-response curve of the complex I inhibitor rotenone on ROS generation, as measured by rhodamine 123 (Rh123) fluorescence, was much more pronounced than that of rotenone on mitochondrial [(3) H]- uptake [which indicates changes in the mitochondrial membrane potential (DeltaPsi (M))]. |
species (ROS) in the human neocortex: role of aging and cognition. Brain Res. 2005 Jul 12;1049(2):147-55.31(0,1,1,1) | Details |
14740892 | Pasdois P, Deveaud C, Voisin P, Bouchaud V, Rigoulet M, Beauvoit B: Contribution of the phosphorylable complex I in the growth phase-dependent respiration of C6 glioma cells in vitro. Biochem J. 2004 May 15;380(Pt 1):193-202. Nevertheless, a quantitative correlation was found between cellular respiration and the rotenone-sensitive NADH ubiquinone oxidoreductase (i.e. complex I) activity. |
10(0,0,1,5) | Details |
11695835 | Chomyn A: Mitochondrial genetic control of assembly and function of complex I in mammalian cells. Circ Res. 2003 Sep 19;93(6):573-80. Epub 2003 Aug 14. Subsequently, we isolated several mutants affected in one or another of the mtDNA-encoded subunits of complex I by exposing established cell lines to high concentrations of rotenone. |
10(0,0,1,5) | Details |
19961238 | Shinzawa-Itoh K, Seiyama J, Terada H, Nakatsubo R, Naoki K, Nakashima Y, Yoshikawa S: Bovine heart NADH-ubiquinone oxidoreductase contains one molecule of with ten isoprene units as one of the cofactors. J Biol Chem. 2005 Nov 25;280(47):39033-41. Epub 2005 Sep 26. The rotenone-sensitive enzymatic activity of the Complex I preparation was comparable to that of Complex I in the mitochondrial membrane. |
9(0,0,1,4) | Details |
19280713 | Chinta SJ, Rane A, Yadava N, Andersen JK, Nicholls DG, Polster BM: Reactive complex I-depleted brain mitochondria. Free Radic Biol Med. 2009 Apr 1;46(7):939-47. Isolated Hq brain mitochondria oxidizing complex I substrates displayed no difference compared to wild type (WT) in basal ROS production, H2O2 removal, or ROS production stimulated by complex I inhibitors rotenone or 1-methyl-4-phenylpyridinium. |
species regulation by AIF- and 5(0,0,0,5) | Details |
7948420 | Maklashina EO, Sled' VD, Vinogradov AD: [Hysteresis behavior of complex I from bovine heart mitochondria: kinetic and thermodynamic parameters of retarded reverse transition from the inactive to active state]. Biokhimiia. 1994 Jul;59(7):946-57. The active form catalyzes the rapid rotenone-sensitive, N-ethylmaleimide-insensitive : Q1 reductase reaction. |
5(0,0,0,5) | Details |
8026508 | De Jong AM, Albracht SP: Ubisemiquinones as obligatory intermediates in the electron transfer from to Plant Mol Biol. 1992 Dec;20(6):1097-110. Until now ubisemiquinones associated with NADH:ubiquinone oxidoreductase (complex I) have been reported to occur in isolated enzyme and in tightly coupled submitochondrial particles. The EPR signal of the rotenone-sensitive ubisemiquinones could be detected not only in coupled MgATP submitochondrial particles, but also in routine preparations of uncoupled submitochondrial particles and in mitochondria. |
3(0,0,0,3) | Details |
19526285 | Mallajosyula JK, Chinta SJ, Rajagopalan S, Nicholls DG, Andersen JK: Metabolic control analysis in a cellular model of elevated MAO-B: relevance to Parkinson's disease. J Biol Chem. 2000 Dec 1;275(48):37774-8. MAO-B mediated increases in H (2) O (2) also appeared to result in direct oxidative inhibition of both mitochondrial complex I and aconitase. |
3(0,0,0,3) | Details |
18182110 | Hoegger MJ, Lieven CJ, Levin LA: Differential production of by neuronal mitochondria. . J Clin Endocrinol Metab. 2010 Feb;95(2):894-902. Epub 2009 Dec 18. For example, Leber's hereditary optic neuropathy (LHON) results from one of three point mutations mtDNA coding for complex I components, but is only manifested in retinal ganglion cells (RGCs), a central neuron contained within the retina. Cerebral but not RGC-5 or neuroblastoma cells increased production in response to the complex I inhibitor rotenone, while neuroblastoma but not cerebral or RGC-5 cells dramatically decreased production in response to the complex III inhibitor antimycin A. |
3(0,0,0,3) | Details |
386 | Ragan CI, Hinkle PC: Ion transport and respiratory control in vesicles formed from reductase and phospholipids. Mol Biochem Parasitol. 2002 Aug 28;123(2):135-42. NADH-coenzyme Q reductase from bovine heart mitochondria (complex I) was incorporated into phospholipid vesicles by the dialysis procedure. |
2(0,0,0,2) | Details |
11311802 | Dedov VN, Mandadi S, Armati PJ, Verkhratsky A: mitochondria in dorsal root ganglion neurons is enhanced by vanilloid receptors. Neuroscience. 2001;103(1):219-26. Rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, and oligomycin, an inhibitor of F (0) F (1)-ATPase, significantly enhanced the mitochondrial depolarisation produced by in DRG neurons. Rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, and oligomycin, an inhibitor of F (0) F (1)-ATPase, significantly enhanced the mitochondrial depolarisation produced by in DRG neurons. |
-induced depolarisation of 2(0,0,0,2) | Details |
17289351 | Verkaart S, Koopman WJ, van Emst-de Vries SE, Nijtmans LG, van den Heuvel LW, Smeitink JA, Willems PH: production is inversely related to complex I activity in inherited complex I deficiency. Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):660-5. Epub 2008 Apr 30. In agreement with this finding, rotenone, a potent inhibitor of CI activity, dose-dependently increased production in healthy control cells. |
2(0,0,0,2) | Details |
9588024 | Matsuo M, Endo T, Asada K: Properties of the respiratory NAD (P) H dehydrogenase isolated from the cyanobacterium Synechocystis PCC6803. Plant Cell Physiol. 1998 Mar;39(3):263-7. The enzymatic activity was inhibited by diphenyleneiodonium and salicylhydroxamic acid, but not by rotenone, p-chloromercuribenzoate, N-ethylmaleimide, flavon, dicumarol, or antimycin A. These results suggest that the purified complex is a hydrophilic subcomplex which contains an binding site and flavin, and is dissociated from a hydrophobic subcomplex, which contains binding site. |
1(0,0,0,1) | Details |
12062413 | Svensson AS, Johansson FI, Moller IM, Rasmusson AG: Cold stress decreases the capacity for respiratory oxidation in potato leaves. FEBS Lett. 2002 Apr 24;517(1-3):79-82. The nda1 and ndb1 genes, homologues to genes encoding the non- -pumping respiratory chain NADH dehydrogenases of Escherichia coli and yeast, were compared to genes encoding catalytic subunits of the -pumping NADH dehydrogenase (complex I). This decrease is accompanied by specific decreases of immunodetected NDA protein and internal rotenone-insensitive oxidation in mitochondria isolated from cold-treated plants. |
1(0,0,0,1) | Details |
11566731 | Vernet P, Fulton N, Wallace C, Aitken RJ: Analysis of reactive spermatozoa. Biol Reprod. 2001 Oct;65(4):1102-13. Reverse transcription-polymerase chain reaction analysis indicated that the sperm NAD (P) H oxidoreductase complex is quite distinct from the equivalent leukocyte system. This increase could be blocked by rotenone and oligomycin (R/O) in the presence of or lactate but not |
species generating systems in rat epididymal 1(0,0,0,1) | Details |
19807658 | Choi K, Kim J, Kim GW, Choi C: Oxidative stress-induced necrotic cell death via mitochondira-dependent burst of reactive species. Neurotox Res. 2009 Oct;16(3):186-93. Epub 2009 Mar 5. The inhibition of mitochondrial hyperpolarization by diphenylene iodonium or rotenone, potent inhibitors of mitochondrial respiratory chain complex I, resulted in reduced ROS production and subsequent neuronal cell death in vitro and in vivo. The inhibition of mitochondrial hyperpolarization by diphenylene iodonium or rotenone, potent inhibitors of mitochondrial respiratory chain complex I, resulted in reduced ROS production and subsequent neuronal cell death in vitro and in vivo. |
1(0,0,0,1) | Details |
7904221 | Marey-Semper I, Gelman M, Levi-Strauss M: The high sensitivity to rotenone of striatal uptake suggests the existence of a constitutive metabolic deficiency in dopaminergic neurons from the substantia nigra. Curr Neurovasc Res. 2009 Nov;6(4):213-22. The toxicity of the 1-methyl-4-phenylpyridinium ion (MPP+), an inhibitor of complex I of the respiratory chain, on nigrostriatal dopaminergic neurons contrasts with its relative inefficiency towards other catecholaminergic cell populations in spite of their ability to accumulate this neurotoxin through their high-affinity uptake system. |
1(0,0,0,1) | Details |
9092484 | Miyako K, Kai Y, Irie T, Takeshige K, Kang D: The content of intracellular mitochondrial DNA is decreased by 1-methyl-4-phenylpyridinium ion (MPP+). Neuroscience. 2008 Mar 3;152(1):198-207. On the contrary, 0.1 microM rotenone, which inhibits complex I to the same extent as 25 microM MPP+ in the cells, increases the content of mitochondrial DNA about 2-fold. |
82(1,1,1,2) | Details |
12724545 | Dutilleul C, Garmier M, Noctor G, Mathieu C, Chetrit P, Foyer CH, de Paepe R: Leaf mitochondria modulate whole cell redox homeostasis, set antioxidant capacity, and determine stress resistance through altered signaling and diurnal regulation. J Biol Chem. 2005 Dec 23;280(51):42026-35. Epub 2005 Oct 21. The cytoplasmic male-sterile mutant (CMSII) is impaired in complex I function and displays enhanced nonphosphorylating rotenone-insensitive [NAD (P) H dehydrogenases] and -insensitive (alternative oxidase) respiration. |
82(1,1,1,2) | Details |
16115015 | Sousa SC, Castilho RF: Protective effect of rotenone plus Ca2+-induced mitochondrial oxidative stress and PC12 cell death. J Neurochem. 2003 Sep;86(5):1297-307. Chronic systemic inhibition of mitochondrial respiratory chain complex I by rotenone causes nigrostriatal dopaminergic degeneration in rats, producing an in vivo experimental model of Parkinson's disease. |
on 82(1,1,1,2) | Details |
9379714 | Herrero A, Barja G: Sites and mechanisms responsible for the low rate of free radical production of heart mitochondria in the long-lived pigeon. Biochemistry. 2007 May 29;46(21):6409-16. Epub 2007 May 3. This suggests that the free radical generator of Complex I is located after the ferricyanide reduction site, between the ethoxyformic and the rotenone-sensitive sites. |
81(1,1,1,1) | Details |
15850589 | Rizzardini M, Mangolini A, Lupi M, Ubezio P, Bendotti C, Cantoni L: Low levels of ALS-linked Cu/Zn superoxide dismutase increase the production of reactive species and cause mitochondrial damage and death in motor neuron-like cells. Neuroreport. 2004 Oct 5;15(14):2227-31. The mutant protein rendered G93ASOD1 cells more sensitive to mitochondrial dysfunction induced by stimuli that alter cellular free radical homeostasis, like serum withdrawal, depletion of by ethacrynic acid or rotenone-mediated inhibition of complex I of the mitochondrial electron transport chain. |
81(1,1,1,1) | Details |
16678116 | Chernyak BV, Izyumov DS, Lyamzaev KG, Pashkovskaya AA, Pletjushkina OY, Antonenko YN, Sakharov DV, Wirtz KW, Skulachev VP: Production of reactive species in mitochondria of HeLa cells under oxidative stress. Mol Neurodegener. 2008 Dec 29;3:21. In living cells, MR-mediated PDT initiates a delayed ("dark") accumulation of ROS, which is accelerated by inhibitors of the respiratory chain (piericidin, rotenone and myxothiazol) and inhibited by MitoQ and diphenyleneiodonium (an inhibitor of flavin enzymes), indicating that flavin of Complex I is involved in the ROS production. |
81(1,1,1,1) | Details |
15710606 | Zoccarato F, Toscano P, Alexandre A: complex I: stimulation by rotenone, control by Ca (2+), and relevance to Parkinson disease. FEBS Lett. 1991 Nov 4;292(1-2):289-92. Inhibitors of Complex I of the mitochondrial respiratory chain, such as rotenone, promote Parkinson disease-like symptoms and signs of oxidative stress. |
-derived dopaminochrome promotes H (2) O (2) release at mitochondrial 69(0,2,3,4) | Details |
8595975 | Soole KL, Menz RI: Functional molecular aspects of the NADH dehydrogenases of plant mitochondria. J Cereb Blood Flow Metab. 1997 Mar;17(3):265-72. As well as complex I, plant mitochondria contain several type-II NAD (P) H dehydrogenases which mediate rotenone-insensitive oxidation of cytosolic and matrix |
35(0,1,1,5) | Details |
10417649 | Krebs W, Steuber J, Gemperli AC, Dimroth P: Na+ translocation by the NADH:ubiquinone oxidoreductase (complex I) from Klebsiella pneumoniae. Nutr Metab Cardiovasc Dis. 2010 Mar 12. The uptake of ions was severely inhibited by the complex I-specific inhibitor rotenone with deaminoNADH or as substrate. |
35(0,1,1,5) | Details |
8585613 | Blandini F, Greenamyre JT: Assay of [3H] dihydrorotenone binding to complex I in intact human platelets. J Neurosci. 2004 Sep 8;24(36):7779-88. We have developed an assay for the binding of [3H]-dihydrorotenone ([3H] DHR), an analogue of the pesticide rotenone, to the mitochondrial enzyme, complex I, in intact human platelets. |
33(0,1,1,3) | Details |
11080300 | Sabar M, De Paepe R, de Kouchkovsky Y: Complex I impairment, respiratory compensations, and photosynthetic decrease in nuclear and mitochondrial male sterile mutants of Nicotiana sylvestris. Ann Rheum Dis. 1995 Jun;54(6):491-3. We have previously shown that in Nicotiana sylvestris cytoplasmic male-sterile (CMS) mutants where the mtDNA lacks the nad7 gene coding for a subunit of respiratory Complex I (NADH:ubiquinone oxidoreductase, EC 1.6.5.3), (Gly) oxidation was lower than in the wild type and insensitive to rotenone, suggesting Complex I dysfunction. |
33(0,1,1,3) | Details |
10989660 | Greenamyre JT, MacKenzie G, Peng TI, Stephans SE: Mitochondrial dysfunction in Parkinson's disease. Biochim Biophys Acta. 2007 Sep;1772(9):1041-51. Epub 2007 May 25. We developed a novel model of PD in which chronic, systemic infusion of rotenone, a complex-I inhibitor, selectively kills dopaminergic nerve terminals and causes retrograde degeneration of substantia nigra neurons over a period of months. |
32(0,1,1,2) | Details |
15890007 | Dukes AA, Korwek KM, Hastings TG: The effect of endogenous rotenone-induced toxicity in PC12 cells. Biochim Biophys Acta. 2010 Apr;1797(4):509-515. Epub 2010 Jan 25. Systemic exposure to rotenone, a Complex I inhibitor, has been shown to lead to selective dopaminergic cell death in vivo and toxicity in many in vitro models, including dopaminergic cell cultures. |
in 32(0,1,1,2) | Details |
17041725 | Liu YY, Zhao HY, Zhao CL, Duan CL, Lu LL, Yang H: [Overexpression of alpha-synuclein in SH-SY5Y cells partially protected against oxidative stress induced by rotenone]. Stroke. 1996 Feb;27(2):327-31; discussion 332. After treatment with rotenone, both cell viability and complex I activity in these cells were reduced in a concentration-dependent manner. |
32(0,1,1,2) | Details |
19889626 | Olson ML, Chalmers S, McCarron JG: Mitochondrial Ca2+ uptake increases Ca2+ release from receptor clusters in smooth muscle cells. PLoS One. 2009 May 27;4(5):e5701. The protonophore carbonyl 3-chloropheylhydrazone and complex I inhibitor rotenone each depolarized DeltaPsi (M) to prevent mitochondrial Ca2+ uptake and attenuated Ca2+ puffs by approximately 66 or approximately 60%, respectively. |
31(0,1,1,1) | Details |
18562315 | Sugeno N, Takeda A, Hasegawa T, Kobayashi M, Kikuchi A, Mori F, Wakabayashi K, Itoyama Y: Serine 129 phosphorylation of alpha-synuclein induces unfolded protein response-mediated cell death. Ann N Y Acad Sci. 2008 Dec;1148:530-5. Following the treatment with rotenone, a mitochondrial complex I inhibitor, wild type alpha-synuclein-overexpressing cells demonstrated intracellular aggregations, which shared a number of features with Lewy bodies, although cells overexpressing the S129A mutant, in which phosphorylation at Ser (129) was blocked, showed few aggregations. |
31(0,1,1,1) | Details |
8720174 | Santhamma KR, Bhaduri A: Characterization of the respiratory chain of Leishmania donovani promastigotes. FEBS Lett. 2003 Aug 28;550(1-3):163-7. Inhibition analysis of respiration of Leishmania donovani promastigotes in resting, starved and permeabilized cells in the presence of classical electron transfer complex inhibitors such as rotenone, thenoyltrifluoroacetone and antimycin demonstrated the absence of complex I component of the respiratory chain in this organism. |
31(0,1,1,1) | Details |
18832013 | Kim HY, Chung JM, Chung K: Increased production of mitochondrial in the spinal cord induces pain behaviors in mice: the effect of mitochondrial electron transport complex inhibitors. Exp Mol Pathol. 2004 Dec;77(3):210-3. The levels of mechanical hyperalgesia after antimycin A, a complex III inhibitor, were higher than that with rotenone, a complex I inhibitor. |
31(0,1,1,1) | Details |
16990510 | Chen Q, Moghaddas S, Hoppel CL, Lesnefsky EJ: Reversible blockade of electron transport during ischemia protects mitochondria and decreases myocardial injury following reperfusion. Mol Biochem Parasitol. 1995 Dec;75(1):43-53. The reversible blockade of electron transport during ischemia with amobarbital, an inhibitor at the rotenone site of complex I, protects mitochondria against ischemic damage. |
31(0,1,1,1) | Details |
14580324 | Zuo L, Pasniciuc S, Wright VP, Merola AJ, Clanton TL: Sources for blockade of electron transport, oxidase, and anion channels in diaphragm. Brain Res. 1997 Apr 4;753(1):157-62. The mitochondria within intact rat diaphragm were inhibited at complex I (amobarbital or rotenone) or complex I and II (rotenone plus thenoyltrifluoroacetone). |
release: lessons from 31(0,1,1,1) | Details |
14697328 | Bonsi P, Calabresi P, De Persis C, Papa M, Centonze D, Bernardi G, Pisani A: Early ionic and membrane potential changes caused by the pesticide rotenone in striatal cholinergic interneurons. Antioxid Redox Signal. 2003 Oct;5(5):667-75. Acute application of the mitochondrial complex I inhibitor rotenone produced an early membrane hyperpolarization coupled to a fall in input resistance, followed by a late depolarizing response. |
31(0,1,1,1) | Details |
7988736 | Bereznowski Z: Effect of methyl methacrylate on mitochondrial function and structure. Eur J Biochem. 1996 Oct 1;241(1):280-5. The data presented suggest that in the isolated mitochondria MM inhibits oxidation in the vicinity of the rotenone sensitive site of complex I. 7. |
31(0,1,1,1) | Details |
11454754 | Remacle C, Baurain D, Cardol P, Matagne RF: Mutants of Chlamydomonas reinhardtii deficient in mitochondrial complex I: characterization of two mutations affecting the nd1 coding sequence. Plant Physiol. 2009 Jul;150(3):1286-96. Epub 2009 May 29. The mitochondrial rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) comprises more than 30 subunits, the majority of which are encoded by the nucleus. |
9(0,0,1,4) | Details |
8761491 | Buchanan SK, Walker JE: Large-scale chromatographic purification of F1F0-ATPase and complex I from bovine heart mitochondria. J Neural Transm. 2009 Jul;116(7):791-806. Epub 2009 Jun 6. The complex I preparation contains all of the subunits identified in other preparations of the enzyme, and has rotenone-sensitive NADH:ubiquinone oxidoreductase and NADH:ferricyanide oxidoreductase activities. |
9(0,0,1,4) | Details |
9711297 | Miyoshi H, Ohshima M, Shimada H, Akagi T, Iwamura H, McLaughlin JL: Essential structural factors of annonaceous acetogenins as potent inhibitors of mitochondrial complex I. Biochim Biophys Acta. 2007 Mar;1772(3):373-81. Epub 2007 Jan 4. These inhibitors act, at the terminal electron transfer step of the enzyme, in a similar way to the usual complex I inhibitors, such as piericidin A and rotenone; however, structural similarities are not apparent between the acetogenins and these known complex I inhibitors. |
5(0,0,0,5) | Details |
17760425 | Grivennikova VG, Kotlyar AB, Karliner JS, Cecchini G, Vinogradov AD: Redox-dependent change of nucleotide affinity to the active site of the mammalian complex I. Eur J Biochem. 2002 Aug;269(16):4020-4. The effect of is completely reversed by rotenone, antimycin A, and uncoupler. |
5(0,0,0,5) | Details |
18037377 | Gostimskaya IS, Grivennikova VG, Cecchini G, Vinogradov AD: Reversible dissociation of bound oxidoreductase (complex I). Osteoarthritis Cartilage. 2006 Oct;14(10):1011-22. Epub 2006 May 5. The catalytic activities of the enzyme, i.e. rotenone-insensitive NADH:hexaammineruthenium III reductase and rotenone-sensitive NADH:quinone reductase decline when bovine heart submitochondrial particles are incubated with in the presence of rotenone or at alkaline pH. |
from the mammalian membrane-3(0,0,0,3) | Details |
9266534 | Ghelli A, Degli Esposti M, Carelli V, Lenaz G: Changes in mitochondrial complex I activity and binding site in Leber's hereditary optic neuropathy (LHON). J Biol Chem. 2004 Dec 10;279(50):51783-92. Epub 2004 Oct 6. Both 11778/ND4 and 3460/ND1 mutations induced rotenone resistance and 11778/ND4 showed an increased K (m) for -2 with respect to the control group. |
3(0,0,0,3) | Details |
9718301 | Zickermann V, Barquera B, Wikstrom M, Finel M: Analysis of the pathogenic human mitochondrial mutation ND1/3460, and mutations of strictly conserved residues in its vicinity, using the bacterium Paracoccus denitrificans. Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15136-41. Epub 2008 Sep 23. The human mitochondrial ND1/3460 mutation changes Ala52 to in the ND1 subunit of Complex I, and causes Leber's hereditary optic neuropathy (LHON) [Huoponen et al. (1991) Am. The enzymatic activity of the mutants in the presence of hexammineruthenium (rotenone-insensitive) and (rotenone-sensitive) were assayed. |
3(0,0,0,3) | Details |
15647387 | Koopman WJ, Verkaart S, Visch HJ, van der Westhuizen FH, Murphy MP, van den Heuvel LW, Smeitink JA, Willems PH: Inhibition of complex I of the electron transport chain causes O2-. -mediated mitochondrial outgrowth. J Biol Chem. 2005 Oct 14;280(41):34644-53. Epub 2005 Aug 5. In the present study, we have used rotenone, an inhibitor of complex I of the respiratory chain, which is thought to increase mitochondrial O (2)(-)* production, and mitoquinone (MitoQ), a mitochondria-targeted antioxidant, to investigate the relationship between mitochondrial O (2)(-)* production and morphology in human skin fibroblasts. |
3(0,0,0,3) | Details |
10347173 | Barrientos A, Moraes CT: Titrating the effects of mitochondrial complex I impairment in the cell physiology. Neurosci Lett. 1994 Aug 15;177(1-2):58-62. We used a genetic model (40% CI-inhibited human-ape xenomitochondrial cybrids) and a drug-induced model (0-100% CI-inhibited cells using different concentrations of rotenone). |
2(0,0,0,2) | Details |
16798828 | Andrukhiv A, Costa AD, West IC, Garlid KD: Opening mitoKATP increases complex I of the electron transport chain. J Biol Chem. 1999 Jun 4;274(23):16188-97. Myxothiazol stimulated mitoK (ATP)-dependent ROS production, whereas rotenone had no effect. |
generation from 2(0,0,0,2) | Details |
11543648 | Chen JY, Tsao GC, Zhao Q, Zheng W: Differential cytotoxicity of Mn (II) and Mn (III): special reference to mitochondrial [Fe-S] containing enzymes. Brain. 2004 Oct;127(Pt 10):2183-92. Epub 2004 Sep 1. In contrast, rotenone and MPP+ did not seem to alter mtDNA levels. Following exposure of mitochondrial fractions with Mn (II) or Mn (III), there was a significant inhibition by either Mn species in activities of Complex I whose active site contains five to eight [Fe-S] clusters. |
2(0,0,0,2) | Details |
11337409 | Moller IM: PLANT MITOCHONDRIA AND OXIDATIVE STRESS: Electron Transport, Turnover, and Metabolism of Reactive Species. Trans Am Ophthalmol Soc. 2007;105:379-91. In addition to complexes I-IV, the plant mitochondrial ETC contains a non- -pumping alternative oxidase as well as two rotenone-insensitive, non- -pumping NAD (P) H dehydrogenases on each side of the inner membrane: NDex on the outer surface and NDin on the inner surface. Complex I is the main enzyme oxidizing under normal conditions and is also a major site of ROS production, together with complex III. |
1(0,0,0,1) | Details |
14706836 | Talbot DA, Lambert AJ, Brand MD: Production of endogenous matrix from mitochondrial complex I leads to activation of uncoupling protein 3. J Biol Chem. 2007 Aug 17;282(33):24146-56. Epub 2007 Jun 20. Both production and the GDP-sensitive conductance were suppressed by rotenone plus an antioxidant. |
1(0,0,0,1) | Details |
8285590 | Dexter DT, Sian J, Rose S, Hindmarsh JG, Mann VM, Cooper JM, Wells FR, Daniel SE, Lees AJ, Schapira AH, et al.: Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease. Ann Neurol. 1994 Jan;35(1):38-44. There may be some impairment of mitochondrial complex I activity in the substantia nigra in Parkinson's disease.(ABSTRACT TRUNCATED AT 250 WORDS) Rotenone-sensitive reductase activity (complex I) was reduced to levels intermediate between those in control subjects and those in patients with overt Parkinson's disease, but this change did not reach statistical significance. |
1(0,0,0,1) | Details |
8135820 | Pecci L, Montefoschi G, Fontana M, Cavallini D: Aminoethylcysteine ketimine decarboxylated dimer inhibits mitochondrial respiration by impairing electron transport at complex I level. Steroids. 2006 Nov;71(11-12):984-92. Epub 2006 Sep 6. Furthermore, the dimer did not affect the rotenone-insensitive electron transfer from to |
1(0,0,0,1) | Details |
17239993 | Tsuruta T, Oh-Hashi K, Ueno Y, Kitade Y, Kiuchi K, Hirata Y: RNAi knockdown of caspase-activated DNase inhibits rotenone-induced DNA fragmentation in HeLa cells. Biochim Biophys Acta. 2001 Apr 2;1504(2-3):179-95. Rotenone, an inhibitor of mitochondrial complex I, induces apoptosis in a variety of cells. |
1(0,0,0,1) | Details |
16668682 | Soole KL, Dry IB, Wiskich JT: Partial Purification and Characterization of Complex I, NADH:Ubiquinone Reductase, from the Inner Membrane of Beetroot Mitochondria. Eur J Neurosci. 1993 Aug 1;5(8):1029-34. The purified NADH dehydrogenase complex catalyzed the reduction of various electron acceptors with as the electron donor, was not sensitive to rotenone inhibition, and had a slow - reductase activity. |
1(0,0,0,1) | Details |
11100151 | Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT: Chronic systemic pesticide exposure reproduces features of Parkinson's disease. Plant Cell. 2003 May;15(5):1212-26. We report that chronic, systemic inhibition of complex I by the lipophilic pesticide, rotenone, causes highly selective nigrostriatal dopaminergic degeneration that is associated behaviorally with hypokinesia and rigidity. |
82(1,1,1,2) | Details |
15704879 | Bufetov EN, Polygalova OO, Ponomareva AA: [Ultrastructural characteristics of mitochondria during cell adaptation to rotenone]. J Biol Chem. 2006 Mar 17;281(11):7136-42. Epub 2006 Jan 12. A study was made of respiration, heat production, K+ output and ultrastructure of wheat root cells treated for 6 h with rotenone (10 microM), an inhibitor of HADH- oxidoreductase (Complex I). |
81(1,1,1,1) | Details |
17579777 | Cao Q, Wei LR, Lu LL, Zhao CL, Zhao HY, Yang H: Astrocytes protect MN9D neuronal cells against rotenone-induced oxidative stress by a -dependent mechanism. FEBS Lett. 1994 Feb 14;339(1-2):142-6. Rotenone specifically inhibits mitochondrial complex I, and long exposure to rotenone may increase the risk for Parkinson's disease (PD) and cause Parkinsonism. |
81(1,1,1,1) | Details |
19059197 | Fato R, Bergamini C, Bortolus M, Maniero AL, Leoni S, Ohnishi T, Lenaz G: Differential effects of mitochondrial Complex I inhibitors on production of reactive species. Ukr Biokhim Zh. 2003 Nov-Dec;75(6):115-22. Our results indicate that different Complex I inhibitors can be grouped into two classes: Class A inhibitors (Rotenone, Piericidin A and Rolliniastatin 1 and 2) increase ROS production; Class B inhibitors (Stigmatellin, Mucidin, and (2)) prevent ROS production also in the presence of Class A inhibitors. |
65(0,2,2,5) | Details |
14598303 | Shamoto-Nagai M, Maruyama W, Kato Y, Isobe K, Tanaka M, Naoi M, Osawa T: An inhibitor of mitochondrial complex I, rotenone, inactivates proteasome by oxidative modification and induces aggregation of oxidized proteins in SH-SY5Y cells. FEBS Lett. 1996 Feb 12;380(1-2):176-8. |
63(0,2,2,3) | Details |
17601793 | Merker MP, Audi SH, Lindemer BJ, Krenz GS, Bongard RD: Role of mitochondrial electron transport complex I in reduction by intact pulmonary arterial endothelial cells and the effect of hyperoxia. Parasitol Int. 2005 Sep;54(3):185-93. The mitochondrial electron transport complex I inhibitor rotenone decreased the CoQ (1) reduction rate by 85% in the normoxic cells and 44% in the hyperoxia-exposed cells. |
34(0,1,1,4) | Details |
17706244 | de Wit LE, Spruijt L, Schoonderwoerd GC, de Coo IF, Smeets HJ, Scholte HR, Sluiter W: A simplified and reliable assay for complex I in human blood lymphocytes. . J Nucl Med. 1997 Jul;38(7):1155-60. The results of the present study show that permeabilization of human blood lymphocytes in the presence of protease inhibitors by three cycles of freeze-thawing enables reproducible detection of the rotenone-sensitive complex I activity. |
34(0,1,1,4) | Details |
10969076 | Lotharius J, O'Malley KL: The parkinsonism-inducing drug 1-methyl-4-phenylpyridinium triggers intracellular oxidation. Am J Physiol Heart Circ Physiol. 2005 Jul;289(1):H243-50. Epub 2005 Mar 11. Although a mean lethal dose of MPP (+) led to ROS production in identified dopaminergic neurons, toxic doses of the Complex I inhibitor rotenone did not. |
33(0,1,1,3) | Details |
7550026 | Charalambous A, Tluczek L, Frey KA, Higgins DS Jr, Greenamyre TJ, Kilbourn MR: Synthesis and biological evaluation in mice of (2-[11C] methoxy)-6',7'-dihydrorotenol, a second generation rotenoid for marking mitochondrial complex I activity. Histochem Cell Biol. 2005 Jul;124(1):69-76. Epub 2005 Jul 22. Recently we reported the synthesis of (2-[11C] methoxy) rotenone ([11C] ROT) as a tool for in vivo studies of complex I. |
33(0,1,1,3) | Details |
15032834 | Hagedorn PH, Flyvbjerg H, Moller IM: Modelling mitochondria. . J Cell Biochem. 2001;82(2):271-6. It is produced by enzymes in, or associated with, the tricarboxylic acid cycle in the matrix, and it is oxidized by two respiratory chain enzymes in the inner membrane, the rotenone-sensitive complex I and the rotenone-insensitive internal NADH dehydrogenase (ND (in)). |
turnover in plant 32(0,1,1,2) | Details |
8627318 | Davey GP, Clark JB: Threshold effects and control of oxidative phosphorylation in nonsynaptic rat brain mitochondria. Am J Physiol Cell Physiol. 2008 Feb;294(2):C460-6. Epub 2007 Dec 12. Rotenone, myxothiazol, and KCN were used to titrate the activities of NADH:ubiquinone oxidoreductase (EC 1.6.5.3; complex I), ubiquinol:ferrocytochrome c oxidoreductase (EC 1.10.2.2; complex III), and cytochrome c oxidase (EC 1.9.3.1; complex IV ), respectively. |
32(0,1,1,2) | Details |
18325346 | MacKenzie EL, Ray PD, Tsuji Y: Role and regulation of ferritin H in rotenone-mediated mitochondrial oxidative stress. J Cell Sci. 2007 Jun 1;120(Pt 11):1908-14. Epub 2007 May 15. Here, we describe a cytoprotective response involving transcriptional activation of the ferritin H gene in response to the mitochondrial complex I inhibitor and compound rotenone. |
31(0,1,1,1) | Details |
7824183 | Brouillet E, Henshaw DR, Schulz JB, Beal MF: Aminooxyacetic acid striatal lesions attenuated by 1,3-butanediol and In the present study, we show that and the specific complex I inhibitor rotenone produces a similar neurochemical profile in the striatum, consistent with an effect of AOAA on energy metabolism. |
J Biol Chem. 2006 May 19;281(20):14250-5. Epub 2006 Mar 16.31(0,1,1,1) | Details |
9932647 | Sreeramulu K, Schmidt CL, Schafer G, Anemuller S: Studies of the electron transport chain of the euryarcheon Halobacterium salinarum: indications for a type II NADH dehydrogenase and a complex III analog. J Bioenerg Biomembr. 1998 Oct;30(5):443-53. Complex I inhibitors like rotenone and annonine were inactive, clearly excluding the presence of a coupled NADH dehydrogenase. |
31(0,1,1,1) | Details |
1399827 | Kawasaki S, Akiyama S, Kurokawa T, Kataoka M, Dohmitsu K, Kondoh K, Yamauchi M, Ito K, Watanabe T, Sugiyama S, et al.: Polyoxyethylene-modified superoxide dismutase reduces side effects of adriamycin and mitomycin C. PLoS One. 2008 Jan 16;3(1):e1433. As for its effective sites, SOD-POE prevented a decrease in the specific activity of rotenone-sensitive - oxido-reductase (complex I) in heart muscle mitochondrial respiratory chain function in BALB/c male mice administered 10 mg/kg ADR, and prevented damage to the sarcoplasmic reticulum and mitochondria of mouse heart muscle by ADR as observed by electron microscopy. |
31(0,1,1,1) | Details |
17513497 | Heinen A, Aldakkak M, Stowe DF, Rhodes SS, Riess ML, Varadarajan SG, Camara AK: Reverse electron flow-induced ROS production is attenuated by activation of mitochondrial Ca2+-sensitive K+ channels. J Appl Physiol. 2007 Aug;103(2):623-8. Epub 2007 Apr 26. It is well known that the (2)-linked substrate induces reverse electron flow to complex I of the electron transport chain and that this process generates (O (2)(*-)); these effects are blocked by the complex I blocker rotenone. |
31(0,1,1,1) | Details |
17880941 | Rojo AI, Cavada C, de Sagarra MR, Cuadrado A: Chronic inhalation of rotenone or paraquat does not induce Parkinson's disease symptoms in mice or rats. J Neurochem. 1996 Jan;66(1):403-11. A new model based on daily inoculation of neurotoxins in the nasal cavity of C57BL/6 mice for 30 days was used to evaluate risk of three complex I inhibitors, 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine (MPTP), rotenone and paraquat. |
31(0,1,1,1) | Details |
1333196 | Ramsay RR, Singer TP: Relation of inhibition of -Q oxidoreductase by rotenone, piericidin A, and MPP+. J Neurosci Res. 2008 Nov 15;86(15):3322-30. The addition of to submitochondrial particles inhibited by agents which interrupt electron transport from -Q oxidoreductase (Complex I) to Q10 (rotenone, piericidin A, and MPP+) results in formation and lipid peroxidation. |
generation and lipid peroxidation to the 31(0,1,1,1) | Details |
19348888 | de Wit LE, Sluiter W: Chapter 9 Reliable assay for measuring complex I activity in human blood lymphocytes and skin fibroblasts. Bioorg Med Chem. 2004 Nov 1;12(21):5525-32. To evaluate a deficiency of complex I activity, biochemical measurements based on estimation of the mitochondrial rotenone-sensitive oxidoreductase activity are an important tool. |
9(0,0,1,4) | Details |
12678433 | Fernandes AS, Pereira MM, Teixeira M: Purification and characterization of the complex I from the respiratory chain of Rhodothermus marinus. Antioxid Redox Signal. 2005 May-Jun;7(5-6):662-72. The rotenone sensitive NADH:menaquinone oxidoreductase (NDH-I or complex I) from the thermohalophilic bacterium Rhodothermus marinus has been purified and characterized. |
9(0,0,1,4) | Details |
2493147 | Ichiki T, Tanaka M, Kobayashi M, Sugiyama N, Suzuki H, Nishikimi M, Ohnishi T, Nonaka I, Wada Y, Ozawa T: Disproportionate deficiency of iron-complex I in mitochondrial encephalomyopathy. Biochemistry. 2010 Jan 26;49(3):487-92. Rotenone-sensitive -cytochrome c reductase activity was found to be decreased in all the tissues examined. |
clusters and subunits of 5(0,0,0,5) | Details |
18414996 | Benit P, Slama A, Rustin P: Decylubiquinol impedes mitochondrial respiratory chain complex I activity. Free Radic Biol Med. 2003 Feb 15;34(4):478-88. |
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19252983 | Racay P, Tatarkova Z, Chomova M, Hatok J, Kaplan P, Dobrota D: Mitochondrial transport and mitochondrial dysfunction after global brain ischemia in rat hippocampus. PLoS One. 2010 Jan 19;5(1):e8762. Ischemia induced progressive inhibition of complex I, affecting final electron transfer to decylubiquinone. |
5(0,0,0,5) | Details |
9163527 | Ghelli A, Benelli B, Esposti MD: Measurement of the membrane potential generated by complex I in submitochondrial particles. J Biol Chem. 2008 Oct 24;283(43):29292-300. Epub 2008 Aug 7. |
5(0,0,0,5) | Details |
12069106 | Chan TS, Teng S, Wilson JX, Galati G, Khan S, O'Brien PJ: complex I cytopathies involves NAD (P) H: quinone oxidoreductase 1 (NQO1). Pigment Cell Res. 2003 Oct;16(5):553-9. In the following, using hepatocytes as a model cell, we have shown for the first time that the cytotoxicity caused by complex I inhibition by rotenone but not that caused by complex III inhibition by antimycin can be prevented by (CoQ1) or |
cytoprotective mechanisms for mitochondrial 5(0,0,0,5) | Details |
11960602 | Detaille D, Guigas B, Leverve X, Wiernsperger N, Devos P: Obligatory role of membrane events in the regulatory effect of function. Toxicol Sci. 2004 May;79(1):137-46. Epub 2004 Feb 19. From recent findings about the indirect effect of (MET) targeted on the respiratory chain complex I, we reconsidered this question and tried to determine the causality of any alteration at this enzymatic level using Xenopus laevis oocytes. Addition of MET (50 microM) reduced by 40% the rotenone-sensitive activity of complex I only in incubating intact oocytes but not in mitochondria isolated by differential centrifugation. |
on the respiratory chain 3(0,0,0,3) | Details |
16818739 | Yi JS, Holbrook BC, Michalek RD, Laniewski NG, Grayson JM: Electron transport complex I is required for CD8+ T cell function. . FEBS Lett. 1997 Jun 30;410(2-3):467-9. To block mitochondrial function, transgenic CD8+ T cells were incubated with increasing doses of rotenone, an inhibitor of electron transport complex I. |
3(0,0,0,3) | Details |
16410242 | Schonfeld P, Reiser G: Rotenone-like action of the branched-chain induces oxidative stress in mitochondria. Neurochem Res. 2009 Apr;34(4):746-54. Epub 2008 Sep 19. With alone, Phyt suppresses O (2)(.) generation caused by reverse electron transport from to complex I. |
2(0,0,0,2) | Details |
18615737 | Sala G, Trombin F, Beretta S, Tremolizzo L, Presutto P, Montopoli M, Fantin M, Martinuzzi A, Carelli V, Ferrarese C: Antioxidants partially restore transport defect in leber hereditary optic neuropathy cybrids. J Neurosci Res. 2008 Nov 15;86(15):3331-7. Despite the important role of respiratory chain deficiency and oxidative stress induced by mtDNA point mutations affecting complex I, excitotoxic injury has been postulated as a concurrent pathogenic factor. Rotenone, a classic complex I inhibitor, did not worsen the uptake defect present in LHON cybrids under basal conditions but significantly reduced transport in control cybrids. |
2(0,0,0,2) | Details |
20307667 | Greene JG, Dingledine R, Greenamyre JT: Neuron-selective changes in RNA transcripts related to energy metabolism in toxic models of parkinsonism in rodents. Biochem J. 2004 Sep 1;382(Pt 2):511-7. Mitochondrial complex I inhibition by rotenone or MPTP can induce SNDA neurodegeneration and recapitulate motor disability in rodents. We performed a transcriptional analysis of the midbrain response to complex I inhibition focused on selected metabolic transcripts using quantitative real-time RT-PCR in conjunction with laser-capture microdissection (LCM) of immunofluorescently-targeted SNDA and ventral tegmental area (VTA) DA neurons. |
2(0,0,0,2) | Details |
8804391 | da Silva MV, Alves PC, Duarte M, Mota N, Lobo-da-Cunha A, Harkness TA, Nargang FE, Videira A: Disruption of the nuclear gene encoding the 20.8-kDa subunit of ubiquinone reductase of Neurospora mitochondria. Science. 2007 Jun 1;316(5829):1345-8. The nuclear gene coding for the 20.8-kDa subunit of the membrane arm of respiratory chain ubiquinone reductase (Complex I) from Neurospora crassa, nuo-20.8, was localized on linkage group I of the fungal genome. The ubiquinone reductase activity of sonicated mitochondria from the mutant is rotenone insensitive. |
2(0,0,0,2) | Details |
10717001 | Weinberg JM, Venkatachalam MA, Roeser NF, Nissim I: Mitochondrial dysfunction during hypoxia/reoxygenation and its correction by anaerobic metabolism of cycle intermediates. Biochem Int. 1987 Apr;14(4):735-9. Rotenone, but not antimycin or oligomycin, prevented this effect, indicating that electron transport in complex I, rather than F (1) F (0)-ATPase activity, had been responsible for maintenance of DeltaPsi (m) by the substrates. Thus, tubule cells subjected to hypoxia/reoxygenation can have persistent energy deficits associated with complex I dysfunction for substantial periods of time before onset of the mitochondrial permeability transition and/or loss of cytochrome c. |
2(0,0,0,2) | Details |
9475856 | Yajid F, Mercier JG, Mercier BM, Dubouchaud H, Prefaut C: Effects of 4 wk of hindlimb suspension on skeletal muscle mitochondrial respiration in rats. Free Radic Biol Med. 2000 Jan 15;28(2):235-50. With + rotenone, there was no significant difference in the respiratory rate compared with the respective control group, whatever the mitochondrial origin (SS, or IMF, or from single muscle). We conclude that 4 wk of hindlimb suspension alters the respiration of IMF mitochondria in hindlimb skeletal muscles and seems to act negatively on complex I of the electron-transport chain or prior sites. |
1(0,0,0,1) | Details |
17428841 | Koopman WJ, Verkaart S, Visch HJ, van Emst-de Vries S, Nijtmans LG, Smeitink JA, Willems PH: Human NADH:ubiquinone oxidoreductase deficiency: radical changes in mitochondrial morphology?. Neuroscience. 2007 Jul 13;147(3):592-8. Epub 2007 Jun 20. Malfunction of NADH:ubiquinone oxidoreductase or complex I (CI), the first and largest complex of the mitochondrial oxidative phosphorylation system, has been implicated in a wide variety of human disorders. |
1(0,0,0,1) | Details |
15337616 | Kaplanova V, Zeman J, Hansikova H, Cerna L, Houst'kova H, Misovicova N, Houstek J: Segregation pattern and biochemical effect of the G3460A mtDNA mutation in 27 members of LHON family. J Biol Chem. 2001 Oct 19;276(42):38808-13. Epub 2001 Jul 30. Although enzyme assay showed reduction of complex I activity, our results give additional support to the hypothesis that expression of LHON mutation depends on complex nuclear-mitochondrial interaction. |
1(0,0,0,1) | Details |
7941733 | Buschges R, Bahrenberg G, Zimmermann M, Wolf K: The strictly aerobic yeasts Candida pinus, Cryptococcus albidus, Rhodotorula minuta, Rhodotorula mucilaginosa and Trichosporon beigelii possess mitochondrial NADH dehydrogenases with significant features of the NADH:ubiquinone oxidoreductase (complex I). These species show in all growth phases and under standard cultivation conditions, NADH dehydrogenases of approximately 700 kDa, which are sensitive to rotenone, a specific inhibitor of this complex. |
oxidoreductase in obligate aerobic yeasts. J Neurochem. 1994 Nov;63(5):1987-90.1(0,0,0,1) | Details |
20095467 | Cheng Y, Ren M, Niu Y, Qiao J, Aneba S, Chorvat D Jr, Chorvatova A: [Assessment of mitochondrial metabolic oxidative state in living cardiomyocytes with spectrally-resolved fluorescence lifetime spectroscopy of NAD (P) H]. Plant Physiol. 1992 Feb;98(2):588-594. Rotenone, the inhibitor of Complex I of the mitochondrial respiratory chain, increased AF intensity and shortened the average fluorescence lifetime. Rotenone, the inhibitor of Complex I of the mitochondrial respiratory chain, increased AF intensity and shortened the average fluorescence lifetime. |
1(0,0,0,1) | Details |
9256232 | Igamberdiev AU, Bykova NV, Gardestrom P: Involvement of rotenone-insensitive pathways of mitochondrial electron transport during oxidation of in higher plants. Neurosci Lett. 2009 Jul 31;459(1):11-5. Epub 2009 May 4. The involvement of different paths of electron transport in mitochondria during operation of glycine decarboxylase complex (GDC) was tested in different conditions, using aminoacetonitrile (AAN), the inhibitor of oxidation in mitochondria, rotenone, the inhibitor of Complex I of mitochondrial electron transport, and inhibitors of cytochrome oxidase and alternative oxidase. |
-resistant and 1(0,0,0,1) | Details |
9449429 | Nakao N, Nakai K, Itakura T: Metabolic inhibition enhances selective toxicity of toward mesencephalic neurons in vitro. J Appl Physiol. 2008 Dec;105(6):1706-13. Epub 2008 Sep 18. We investigated whether metabolic inhibition with rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, may enhance the toxicity of toward DA neurons in mesencephalic cultures. We investigated whether metabolic inhibition with rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, may enhance the toxicity of toward DA neurons in mesencephalic cultures. |
1(0,0,0,1) | Details |
16085644 | Shang T, Joseph J, Hillard CJ, Kalyanaraman B: Death-associated protein kinase as a sensor of mitochondrial membrane potential: role of lysosome in mitochondrial toxin-induced cell death. Free Radic Biol Med. 2001 Nov 15;31(10):1216-27. We have investigated here the mechanism of dephosphorylation and activation of death-associated protein kinase (DAPK) and the role of lysosome in neuroblastoma cells (SH-SY5Y) treated with mitochondrial toxins, such as MPP (+) and rotenone. Complex I inhibition by mitochondrial toxins (e.g. |
1(0,0,0,1) | Details |
15111504 | Ye G, Metreveli NS, Donthi RV, Xia S, Xu M, Carlson EC, Epstein PN: Catalase protects cardiomyocyte function in models of type 1 and type 2 diabetes. Biochim Biophys Acta. 2002 Feb 15;1553(3):249-60. Chronic overexpression of catalase or acute in vitro treatment with rotenone, an inhibitor of mitochondrial complex I, or thenoyltrifluoroacetone, an inhibitor of mitochondrial complex II, eliminated excess ROS production in diabetic cardiomyocytes. Chronic overexpression of catalase or acute in vitro treatment with rotenone, an inhibitor of mitochondrial complex I, or thenoyltrifluoroacetone, an inhibitor of mitochondrial complex II, eliminated excess ROS production in diabetic cardiomyocytes. |
1(0,0,0,1) | Details |
8875956 | Corsini E, Schubert C, Marinovich M, Galli CL: Role of mitochondria in tributyltin-induced interleukin-1alpha production in murine keratinocytes. Neuroscience. 2005;135(4):1087-94. Epub 2005 Sep 8. TBT induced a direct and concentration-related activation of NF-(kappa) B, which peaked at 2 h and was blocked by pyrrolidinedithiocarbamate, a potent NF-(kappa) B inhibitor, and rotenone, an inhibitor of the electron entry from complex I to TBT induced a direct and concentration-related activation of NF-(kappa) B, which peaked at 2 h and was blocked by pyrrolidinedithiocarbamate, a potent NF-(kappa) B inhibitor, and rotenone, an inhibitor of the electron entry from complex I to |
1(0,0,0,1) | Details |
4039407 | Mendis AH, Townson S: Evidence for the occurrence of respiratory electron transport in adult Brugia pahangi and Dipetalonema viteae. Eur J Biochem. 2003 Dec;270(24):4942-51. When assayed as separate unisexual groups, the uptake of male and female macrofilariae of both species was inhibited by classical inhibitors of respiratory electron transport (RET), and showed classical substrate bypass phenomena in response to and N,N,N',N'-tetramethyl-p-phenylenediamine with respect to the RET inhibitors rotenone (inhibitor of complex I) and antimycin A (inhibitor of complex III). When assayed as separate unisexual groups, the uptake of male and female macrofilariae of both species was inhibited by classical inhibitors of respiratory electron transport (RET), and showed classical substrate bypass phenomena in response to and N,N,N',N'-tetramethyl-p-phenylenediamine with respect to the RET inhibitors rotenone (inhibitor of complex I) and antimycin A (inhibitor of complex III). |
1(0,0,0,1) | Details |
19067348 | Mortiboys H, Thomas KJ, Koopman WJ, Klaffke S, Abou-Sleiman P, Olpin S, Wood NW, Willems PH, Smeitink JA, Cookson MR, Bandmann O: Mitochondrial function and morphology are impaired in parkin-mutant fibroblasts. Mol Biochem Parasitol. 1985 Mar;14(3):337-54. RESULTS: Parkin-mutant cells had lower mitochondrial complex I activity and complex I-linked production, which correlated with a greater degree of mitochondrial branching, suggesting that the functional and morphological effects of parkin are related. Fluorescence recovery after photobleaching assays demonstrated a lower level of functional connectivity of the mitochondrial matrix, which further worsened after rotenone exposure. |
1(0,0,0,1) | Details |
19232380 | Kawasaki A, Hayashi T, Nakachi K, Trosko JE, Sugihara K, Kotake Y, Ohta S: Modulation of connexin 43 in rotenone-induced model of Parkinson's disease. Neuroscience. 2009 Apr 21;160(1):61-8. Epub 2009 Feb 13. In this study, we show that a major gap junctional protein, connexin43 (Cx43), in astrocytes is enhanced both in a rat Parkinson's disease (PD) model induced with rotenone, a widely used pesticide that inhibits mitochondrial complex I, and in vitro in cultured astrocytes stimulated with rotenone. |
81(1,1,1,1) | Details |
16666054 | Day DA, Moore AL, Dry IB, Wiskich JT, Azcon-Bieto J: Regulation of Nonphosphorylating Electron Transport Pathways in Soybean Cotyledon Mitochondria and Its Implications for Fat Metabolism. EMBO J. 1998 Aug 17;17(16):4848-58. Despite substantial rotenone-resistant O (2) uptake with NAD-linked substrates, respiratory control was observed in the presence of antimycin, indicating restriction of electron flow through complex I. |
81(1,1,1,1) | Details |
17298981 | Benard G, Bellance N, James D, Parrone P, Fernandez H, Letellier T, Rossignol R: Mitochondrial bioenergetics and structural network organization. Eur J Biochem. 1987 Dec 15;169(3):585-91. Second, we followed the effect of rotenone, a specific inhibitor of respiratory chain complex I, which causes large structural perturbations, once a threshold was reached. |
81(1,1,1,1) | Details |
19495970 | Villa RF, Gorini A, Hoyer S: Effect of Ageing and Ischemia on Enzymatic Activities Linked to Krebs' Cycle, Electron Transfer Chain, and Aminoacids Metabolism of Free and Intrasynaptic Mitochondria of Cerebral Cortex. Neurosci Lett. 2002 Nov 15;333(1):25-8. The maximum rate (V (max)) of the following enzyme activities: citrate synthase, malate dehydrogenase, succinate dehydrogenase for Krebs' cycle; -cytochrome c reductase as total (integrated activity of Complex I-III), rotenone sensitive (Complex I) and cytochrome oxidase (Complex IV) for electron transfer chain; dehydrogenase, - - and glutamate-pyruvate transaminases for glutamate metabolism were assayed in non-synaptic, perikaryal mitochondria and in two populations of intra-synaptic mitochondria, i.e., the light and heavy mitochondrial fraction. |
81(1,1,1,1) | Details |
6713449 | Quinn PJ, Crutcher EC: The action of beta-adrenoceptor antagonists on rat heart mitochondrial function in vitro: a comparison of timolol, and Cardiovasc Res. 1984 Apr;18(4):212-9. Transfer of electrons through Complex I measured by the rate of reduction of ferricyanide by submitochondrial particles inhibited by rotenone and the lack of specific inhibition by of supported respiration indicated that one site of drug action was between NADH dehydrogenase and its associated flavoprotein, possibly close to the site of rotenone inhibition. |
81(1,1,1,1) | Details |
1932041 | Bironaite DA, Cenas NK, Kulys JJ: The rotenone-insensitive reduction of quinones and nitrocompounds by mitochondrial NADH:ubiquinone reductase. Biochemistry. 2008 Oct 7;47(40):10816-26. Epub 2008 Sep 10. The rotenone-insensitive reduction of quinones and aromatic nitrocompounds by mitochondrial ubiquinone reductase (complex I, EC 1.6.99.3) has been studied. |
81(1,1,1,1) | Details |
12097231 | Li C, Wright MM, Jackson RM: Reactive species mediated injury of human lung epithelial cells after hypoxia-reoxygenation. Neurobiol Dis. 2010 Mar 19. Rotenone and myxothiazole increased DCF oxidation more in hypoxic than in normoxic cells, suggesting that mitochondrial electron transport complex I may have been altered by hypoxia preexposure. |
81(1,1,1,1) | Details |
11074592 | Gniadecki R, Thorn T, Vicanova J, Petersen A, Wulf HC: Role of mitochondria in ultraviolet-induced oxidative stress. Biochem Biophys Res Commun. 1992 Jul 31;186(2):698-705. The same effect was seen after incubation with rotenone, which blocks electron flow from -reductase (complex I) to |
81(1,1,1,1) | Details |
11527970 | Chauvin C, De Oliveira F, Ronot X, Mousseau M, Leverve X, Fontaine E: Rotenone inhibits the mitochondrial permeability transition-induced cell death in U937 and KB cells. Biochimie. 2002 Dec;84(12):1189-97. Because functional links between the PTP and the respiratory chain complex I have been reported, we have investigated the effects of rotenone on PTP regulation in U937 and KB cells. |
63(0,2,2,3) | Details |
16174799 | Chen Q, Hoppel CL, Lesnefsky EJ: Blockade of electron transport before cardiac ischemia with the reversible inhibitor amobarbital protects rat heart mitochondria. J Pharmacol Exp Ther. 2006 Jan;316(1):200-7. Epub 2005 Sep 20. Irreversible blockade of electron transport at complex I by rotenone decreases ischemic damage to cardiac mitochondria by decreasing the loss of cytochrome c and preserving respiration through cytochrome oxidase. |
62(0,2,2,2) | Details |
11707688 | Yuhki KI, Miyauchi T, Kakinuma Y, Murakoshi N, Maeda S, Goto K, Yamaguchi I, Suzuki T: Endothelin-1 production is enhanced by rotenone, a mitochondrial complex I inhibitor, in cultured rat cardiomyocytes. Brain Res. 2008 Jun 18;1215:208-17. Epub 2008 Apr 12. |
62(0,2,2,2) | Details |
9878712 | Ushakova AV, Grivennikova VG, Ohnishi T, Vinogradov AD: Triton X-100 as a specific inhibitor of the mammalian NADH-ubiquinone oxidoreductase (Complex I). FEMS Yeast Res. 2006 Dec;6(8):1117-29. Also similar to rotenone, Triton X-100 partially protects Complex I against the thermally induced deactivation and partially activates the thermally deactivated enzyme. |
34(0,1,1,4) | Details |
10908294 | Nakamura K, Bindokas VP, Marks JD, Wright DA, Frim DM, Miller RJ, Kang UJ: The selective toxicity of 1-methyl-4-phenylpyridinium to dopaminergic neurons: the role of mitochondrial complex I and reactive species revisited. J Biol Chem. 2004 Jul 23;279(30):31121-30. Epub 2004 May 19. In contrast, the specific complex I inhibitor rotenone, at a dose (20 nM) that was less toxic than MPP (+) to dopaminergic neurons, depolarized DeltaPsim to a greater extent than MPP (+). |
34(0,1,1,4) | Details |
18385062 | He Y, Leung KW, Zhang YH, Duan S, Zhong XF, Jiang RZ, Peng Z, Tombran-Tink J, Ge J: Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants. Eur J Pharmacol. 2001 Nov 16;431(2):163-70. Primary TM cultures were treated with one of the following mitochondrial respiratory chain inhibitors: rotenone (ROT, complex I inhibitor), thenoyltrifluoroacetone (TTFA, complex II inhibitor), myxothiazol or antimycin A (MYX, AM-complex III inhibitors); mitochondrial permeability transition (MPT) inhibitor cyclosporine A (CsA); and antioxidants vitamin E (Vit E) or N-acetylcysteine (NAC). |
33(0,1,1,3) | Details |
14663204 | Sakka N, Sawada H, Izumi Y, Kume T, Katsuki H, Kaneko S, Shimohama S, Akaike A: rotenone. Int J Biochem Cell Biol. 2009 Aug-Sep;41(8-9):1697-707. Epub 2009 Mar 3. We investigated the involvement of and endogenous in neurotoxicity by rotenone, a complex I inhibitor. |
is involved in selectivity of dopaminergic neuronal death by 32(0,1,1,2) | Details |
10515594 | Bailey SM, Pietsch EC, Cunningham CC: Rotenone, a mitochondrial complex I inhibitor that allows electron flow through the (FMN), but prevents electron flow to complex III, significantly increased reactive species production in untreated cells, but decreased reactive species production in antimycin plus -treated cells. |
stimulates the production of reactive oxygen species at mitochondrial complexes I and III. Exp Cell Res. 2001 Oct 15;270(1):56-65.32(0,1,1,2) | Details |
8566093 | Santiago M, Granero L, Machado A, Cano J: Complex I inhibitor effect on the nigral and striatal release of in the presence and absence of nomifensine. Diabetes. 2004 Apr;53(4):1052-9. The effect of inhibitors of complex I respiratory chain--1-methyl-4-phenylpyridinium ion (MPP+, 10 microM) and rotenone (100 microM)--on the release and metabolism of was studied by in vivo microdialysis in the striatum and substantia nigra. |
32(0,1,1,2) | Details |
16449798 | Hsieh CC, Papaconstantinou J: Thioredoxin-ASK1 complex levels regulate ROS-mediated p38 MAPK pathway activity in livers of aged and long-lived Snell dwarf mice. Am J Physiol Heart Circ Physiol. 2006 Nov;291(5):H2067-74. Epub 2006 Jun 23. Here we propose that activation of the p38 MAPK pathway by complex I (CI) generated ROS, in response to rotenone (ROT) treatment, is based on the ability of reduced Trx to bind to and inhibit ASK 1 and its release from the complex upon oxidation. |
31(0,1,1,1) | Details |
12515859 | Miyadera H, Shiomi K, Ui H, Yamaguchi Y, Masuma R, Tomoda H, Miyoshi H, Osanai A, Kita K, Omura S: Atpenins, potent and specific inhibitors of mitochondrial complex II - oxidoreductase). Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):473-7. Epub 2003 Jan 6. The use of specific and potent inhibitors of complex I -ubiquinone reductase) and complex III (ubiquinol-cytochrome c reductase), such as rotenone and antimycin, respectively, has allowed determination of the role of these enzymes in physiological processes. |
31(0,1,1,1) | Details |
10398297 | Duan W, Mattson MP: Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson's disease. Diabetes. 2004 May;53(5):1336-43. The 2-DG treatment suppressed oxidative stress, preserved mitochondrial function, and attenuated cell death in cultured dopaminergic cells exposed to the complex I inhibitor rotenone or Fe2+. 2-DG and DR induced expression of the stress proteins heat-shock protein 70 and -regulated protein 78 in dopaminergic cells, suggesting involvement of these cytoprotective proteins in the neuroprotective actions of 2-DG and DR. |
31(0,1,1,1) | Details |
14766935 | Cheranov SY, Jaggar JH: Mitochondrial modulation of Ca2+ sparks and transient KCa currents in smooth muscle cells of rat cerebral arteries. J Invest Dermatol. 1996 Nov;107(5):720-5. CCCP (a protonophore; 1 microm) and rotenone (an electron transport chain complex I inhibitor; 10 microm) depolarized mitochondria, reduced Ca (2+) spark and wave frequency, and elevated global [Ca (2+)](i) in smooth muscle cells of intact arteries. |
31(0,1,1,1) | Details |
2170057 | Yamamoto M, Akiyama C, Aikawa H: D-penicillamine-induced copper deficiency in suckling mice: neurological abnormalities and brain mitochondrial enzyme activities. J Pharmacol Sci. 2003 Jun;92(2):137-42. Cytochrome c oxidase activity (complex IV) in the brain showed 51% decrease of the controls, on the contrary, rotenone-sensitive cytochrome c reductase (complex I + III) and cytochrome c reductase (complex II + III) were normal. |
31(0,1,1,1) | Details |
19635391 | Monroe RK, Halvorsen SW: Environmental toxicants inhibit neuronal Jak kinase by mitochondrial disruption. Int J Biochem. 1994 Sep;26(9):1119-27. Exposure of BE (2)-C cells to the heavy metals CdCl (2) and HgCl (2) and to the mitochondrial complex I inhibitor rotenone inhibited interleukin-6, interferon-gamma and ciliary neurotrophic factor-mediated Jak/STAT signaling, reduced Jak1 and Jak2 auto-phosphorylation and induced Jak nitration. |
31(0,1,1,1) | Details |
14681995 | Tkachenko HM, Kurhaliuk NM, Vovkanych LS: [Role of ATP-sensitive potassium channel activators in liver mitochondrial function in rats with different resistance to hypoxia]. Biochem J. 2008 Jan 15;409(2):491-9. Additional analyses contain the next inhibitors: mitochondrial fermentative complex I-10 mkM rotenone, succinate dehydrogenase 2 mM |
31(0,1,1,1) | Details |
19520091 | Long J, Ma J, Luo C, Mo X, Sun L, Zang W, Liu J: Comparison of two methods for assaying complex I activity in mitochondria isolated from rat liver, brain and heart. J Neurochem. 2005 Jun;93(5):1199-208. SIGNIFICANCE: Considering the important contribution of the non-specific rotenone-insensitive activity in the complex I assay, it is suggested that the method with BSA addition should be adopted for assaying complex I activity in the brain or liver samples, while the DCIP method is the better choice for heart samples. |
8(0,0,1,3) | Details |
17463293 | Tanaka-Esposito C, Chen Q, Moghaddas S, Lesnefsky EJ: Ischemic preconditioning does not protect via blockade of electron transport. J Pharmacol Exp Ther. 2006 Dec;319(3):1405-12. Epub 2006 Sep 21. Maximally expressed complex I activity measured as rotenone-sensitive NADH:ubiquinone oxidoreductase in detergent-solubilized mitochondria was also unaffected by IPC. |
8(0,0,1,3) | Details |
15248896 | DeHaan C, Habibi-Nazhad B, Yan E, Salloum N, Parliament M, Allalunis-Turner J: Mutation in mitochondrial complex I ND6 subunit is associated with defective response to hypoxia in human glioma cells. Free Radic Biol Med. 1999 Oct;27(7-8):891-900. The T14634C mutation did not abrogate ND6 protein expression, however, M010b cells were more resistant to rotenone, an agent used to screen for Complex I mutations, and adriamycin, an agent activated by redox cycling. |
5(0,0,0,5) | Details |
8294484 | Herz U, Schroder W, Liddell A, Leaver CJ, Brennicke A, Grohmann L: Purification of the NADH:ubiquinone oxidoreductase (complex I) of the respiratory chain from the inner mitochondrial membrane of Solanum tuberosum. J Neurochem. 1993 Oct;61(4):1546-8. The enzyme preparation showed an NADH:ubiquinone-2 reductase activity of 11.5 mumol x min-1 x mg-1 and is strongly inhibited by rotenone. |
5(0,0,0,5) | Details |
10462447 | Tormo JR, Gonzalez MC, Cortes D, Estornell E: Kinetic characterization of mitochondrial complex I inhibitors using annonaceous acetogenins. Neurochem Int. 2007 Jan;50(1):139-47. Epub 2006 Sep 11. |
4(0,0,0,4) | Details |
17339833 | Hinke SA, Martens GA, Cai Y, Finsi J, Heimberg H, Pipeleers D, Van de Casteele M: AMPK-activation and death of pancreatic beta-cells through restoration of mitochondrial electron transfer. Mol Cell Biol. 1995 Feb;15(2):964-74. BACKGROUND AND PURPOSE: Two mechanisms have been proposed to explain the insulin-sensitising properties of in peripheral tissues: (a) inhibition of electron transport chain complex I, and (b) activation of the AMP activated protein kinase (AMPK). In rat beta-cells, caused NAD (P) H accumulation above maximal -inducible levels, mimicking the effect of rotenone. |
antagonises biguanide-induced 4(0,0,0,4) | Details |
15262965 | Lambert AJ, Brand MD: Inhibitors of the -binding site allow rapid production from mitochondrial NADH:ubiquinone oxidoreductase (complex I). J Physiol. 2001 Oct 1;536(Pt 1):211-24. Despite complete inhibition of oxidoreductase activity in each case, different classes of -binding site inhibitor (rotenone, piericidin, and high concentrations of myxothiazol) gave different rates of production during forward electron transport (the rate with myxothiazol was twice that with rotenone) suggesting that the site of rapid generation by complex I is in the region of the -binding sites and not upstream at the flavin or low potential FeS centers. |
4(0,0,0,4) | Details |
7777208 | Blandini F, Porter RH, Greenamyre JT: Autoradiographic study of mitochondrial complex I and glutamate receptors in the basal ganglia of rats after unilateral subthalamic lesion. FEBS J. 2005 Apr;272(7):1649-59. |
3(0,0,0,3) | Details |
14963044 | Batandier C, Leverve X, Fontaine E: Opening of the mitochondrial permeability transition pore induces reactive production at the level of the respiratory chain complex I. J Neurol Neurosurg Psychiatry. 1993 May;56(5):477-80. Moreover, PTP opening decreased rotenone-sensitive ubiquinone reductase activity, whereas it did not affect the FeCN reductase activity. |
species 3(0,0,0,3) | Details |
19821036 | Shiryaeva A, Arkadyeva A, Emelyanova L, Sakuta G, Morozov V: production by the mitochondrial respiratory chain of hepatocytes of rats with experimental toxic hepatitis. FEMS Microbiol Lett. 2004 Aug 1;237(1):139-45. The purpose of this study was to examine our previously formulated assumption concerning the predominant contribution of the complex I to O (2)(*-) production increase by the mitochondrial respiratory chain of hepatocytes in toxic hepatitis (Shiryaeva et al. The rates of O (2)(*-) production by SP of rats with toxic hepatitis in the presence of or rotenone were similar. |
2(0,0,0,2) | Details |
1463844 | Ellersiek U, Steinmuller K: Cloning and transcription analysis of the ndh (A-I-G-E) gene cluster and the ndhD gene of the cyanobacterium Synechocystis sp. J Biol Chem. 2002 Sep 6;277(36):33249-57. Epub 2002 Jun 21. The plastid DNA of higher plants contains eleven reading frames that are homologous to subunits of the mitochondrial NADH-ubiquinone oxidoreductase (complex I). The enzyme is sensitive to rotenone and is located on the cytoplasmic and the thylakoid membrane. |
2(0,0,0,2) | Details |
16357365 | Brueckl C, Kaestle S, Kerem A, Habazettl H, Krombach F, Kuppe H, Kuebler WM: Hyperoxia-induced reactive capillary endothelial cells in situ. Arthritis Rheum. 2003 Mar;48(3):700-8. ROS and [Ca (2+)](i) responses were blocked by the mitochondrial complex I inhibitor rotenone, whereas inhibitors of NAD (P) H oxidase and the intracellular Ca (2+) chelator BAPTA predominantly attenuated the late phase of the hyperoxia-induced DCF fluorescence increase after > 30 min. ROS and [Ca (2+)](i) responses were blocked by the mitochondrial complex I inhibitor rotenone, whereas inhibitors of NAD (P) H oxidase and the intracellular Ca (2+) chelator BAPTA predominantly attenuated the late phase of the hyperoxia-induced DCF fluorescence increase after > 30 min. |
species formation in pulmonary 1(0,0,0,1) | Details |
2539917 | Rossi SC, Wetterhahn KE: reduction of chromate by mitochondrial electron transport chain complexes. J Biol Chem. 1993 Oct 25;268(30):22914-9. Rotenone, antimycin and all produced approximately 40% inhibition of the -dependent chromate-reductase activity. Thus, complex I (NADH:ubiquinone oxidoreductase) appears to be responsible for the inhibitor-insensitive, and complex IV (ferrocytochrome c:oxygen oxidoreductase) for the inhibitor-sensitive -dependent (VI) reduction and (V) formation. |
(V) is produced upon 1(0,0,0,1) | Details |
12013844 | Miki T: [Inhibitors of complex I and II of the mitochondrial respiratory chain] Am J Respir Cell Mol Biol. 2006 Apr;34(4):453-63. Epub 2005 Dec 15. |
1(0,0,0,1) | Details |
17438209 | Tong JJ: Mitochondrial delivery is essential for synaptic potentiation. Somat Cell Mol Genet. 1985 Jul;11(4):345-52. Rotenone, an inhibitor of mitochondrial electron transport chain complex I, suppresses mitochondrial transport and abolishes the potentiation of the synapse. Rotenone, an inhibitor of mitochondrial electron transport chain complex I, suppresses mitochondrial transport and abolishes the potentiation of the synapse. |
1(0,0,0,1) | Details |
11693180 | Yasutake A, Hirayama K: Evaluation of methylmercury biotransformation using rat liver slices. Arch Toxicol. 2001 Sep;75(7):400-6. Rotenone, an inhibitor of complex I in the mitochondrial electron transport system, increased levels of both inorganic Hg and lipid peroxide. Rotenone, an inhibitor of complex I in the mitochondrial electron transport system, increased levels of both inorganic Hg and lipid peroxide. |
1(0,0,0,1) | Details |
10370869 | Zini R, Morin C, Bertelli A, Bertelli AA, Tillement JP: Effects of brain respiratory chain. Mol Microbiol. 1999 Aug;33(3):590-8. This property is especially interesting as this complex is the site where reactive substances (ROS) are generated. The rate of consumption by the different complexes was checked using rotenone (2 microM), (10 mM), antimycin A (1 microM), (KCN) (0.3 mM) and oligomycin (10 microM) to inhibit complexes II, III, IV, V and I, respectively. |
on the rat 1(0,0,0,1) | Details |
18551278 | Lin PC, Puhar A, Steuber J: oxidation drives respiratory Na+ transport in mitochondria from Yarrowia lipolytica. J Bioenerg Biomembr. 1993 Aug;25(4):377-84. -driven Na+ transport was sensitive towards rotenone, a specific inhibitor of complex I. |
82(1,1,1,2) | Details |
15722109 | Capel F, Rimbert V, Lioger D, Diot A, Rousset P, Mirand PP, Boirie Y, Morio B, Mosoni L: Due to reverse electron transfer, mitochondrial H2O2 release increases with age in human vastus lateralis muscle although oxidative capacity is preserved. Neuroreport. 2003 Dec 19;14(18):2425-8. Rotenone abolished this increase, demonstrating that it was due to a free radical release during reverse electron transfer from complex II towards complex I. |
81(1,1,1,1) | Details |
18438923 | Parihar MS, Kunz EA, Brewer GJ: Age-related decreases in NAD (P) H and neurons. Biochem Soc Trans. 1999 Aug;27(4):586-91. With complex I of the electron transport chain inhibited by rotenone, treatment with or ionomycin only resulted in the increase in NAD (P) H fluorescence. |
cause redox declines before ATP loss during treatment of hippocampal 81(1,1,1,1) | Details |
20098733 | Pan-Montojo F, Anichtchik O, Dening Y, Knels L, Pursche S, Jung R, Jackson S, Gille G, Spillantini MG, Reichmann H, Funk RH: Progression of Parkinson's disease pathology is reproduced by intragastric administration of rotenone in mice. J Neurosci. 1995 Sep;15(9):5912-8. Here we report that intragastrically administered rotenone, a commonly used pesticide that inhibits Complex I of the mitochondrial respiratory chain, is able to reproduce PD pathological staging as found in patients. |
81(1,1,1,1) | Details |
19777565 | Deng YT, Huang HC, Lin JK: Rotenone induces apoptosis in MCF-7 human breast cancer cell-mediated ROS through JNK and p38 signaling. J Biol Chem. 1986 Mar 5;261(7):3060-7. Rotenone is an inhibitor of the mitochondrial electron transport chain complex I, resulting in the generation of reactive oxygen species (ROS). |
81(1,1,1,1) | Details |
15143528 | Tkachenko HM, Moibenko OO, Kurhaliuk NM: [Effect of ATP-sensitive potassium channel modulators and intermittent hypoxia on mitochondrial respiration during stress]. J Bioenerg Biomembr. 2003 Oct;35(5):439-50. We used next substrates of oxidation--0.35 mM 1 mM alpha-ketoglutarate, 3 mM 3 mM 2.5 mM and inhibitor of the mitochondrial fermentative complex I (10 microM rotenone), succinate dehydrogenase inhibitor (2 mM and inhibitor of transamination (1 mM aminooxiacetate). |
81(1,1,1,1) | Details |
16004991 | Wang G, Qi C, Fan GH, Zhou HY, Chen SD: PACAP protects neuronal differentiated PC12 cells against the neurotoxicity induced by a mitochondrial complex I inhibitor, rotenone. J Cardiovasc Pharmacol. 2001 Dec;38(6):850-8. |
62(0,2,2,2) | Details |
11358527 | Fang J, Wang Y, Beattie DS: Isolation and characterization of complex I, rotenone-sensitive oxidoreductase, from the procyclic forms of Trypanosoma brucei. Am J Clin Nutr. 2002 Nov;76(5):1031-9. Both proline:cytochrome c reductase and NADH:ubiquinone oxidoreductase of procyclic T. brucei were inhibited by the specific inhibitors of complex I rotenone, piericidin A, and |
44(0,1,3,4) | Details |
12428729 | Stephans SE, Miller GW, Levey AI, Greenamyre JT: Acute mitochondrial and chronic toxicological effects of 1-methyl-4-phenylpyridinium in human neuroblastoma cells. Annu Rev Plant Physiol Plant Mol Biol. 2001 Jun;52:561-591. The lipophilic complex I inhibitor, rotenone, increased excretion in both cell lines. |
38(0,1,2,3) | Details |
3927493 | Garnett KE, Simmons WA, Wing MS, Breen GA: DNA-mediated transfer of complex I genes into three different respiration-deficient Chinese hamster mutant cell lines with defects in complex I of electron transport chain. Yeast. 1994 Apr;10(4):475-9. Evidence for the DNA-mediated transformation of these respiration-deficient cells with a putative complex I gene includes: the clones are respiration-positive and respire at rates comparable to those of wild-type human, hamster, or mouse cells; the clones have rotenone-sensitive oxidase activities, indicating a functional complex I of the electron transport chain; and the clones appear to be true transformants, as demonstrated by hybridization and Southern blot analyses. |
34(0,1,1,4) | Details |
3930501 | Gondal JA, Anderson WM: The molecular morphology of bovine heart mitochondrial ----ubiquinone reductase. J Biol Chem. 1985 Oct 15;260(23):12690-4. Cross-linking of complex I with DSP for 2 min in the presence of 1 microM rotenone yielded a cross-linked product consisting of the two natural disulfide-linked subunits and the 110-115- and 69-kDa polypeptides. |
34(0,1,1,4) | Details |
11714483 | Zhang JG, Nicholls-Grzemski FA, Tirmenstein MA, Fariss MW: hepatocytes against the toxic effect of reactive species generated at mitochondrial complexes I and III by alkylating agents. J Mol Cell Cardiol. 2005 Jul;39(1):149-58. In addition, the treatment with either rotenone (ROT, a complex I inhibitor) or antimycin A (AA, a complex III inhibitor) potentiated EMS-induced lipid peroxidation and necrotic cell death which were again completely prevented by TS treatment. |
protects 32(0,1,1,2) | Details |
11281291 | Schuchmann S, Heinemann U: Increased mitochondrial neurons from trisomy 16 mice: a model of Down's syndrome. Neurotoxicology. 2002 Oct;23(4-5):569-80. In the presence of the mitochondrial respiratory chain complex I inhibitor rotenone production was blocked in diploid neurons, but the increased generation in Ts16 neurons remained. |
generation in 32(0,1,1,2) | Details |
15686486 | Clayton R, Clark JB, Sharpe M: Cytochrome c release from rat brain mitochondria is proportional to the mitochondrial functional deficit: implications for apoptosis and neurodegenerative disease. J Biol Chem. 2000 Dec 8;275(49):38581-8. Titration of rat brain mitochondrial respiratory function, with the specific complex I inhibitor rotenone, caused proportional release of cytochrome c from isolated synaptic and non-synaptic mitochondria. |
32(0,1,1,2) | Details |
18191903 | Greene JG, Greenamyre JT, Dingledine R: Sequential and concerted gene expression changes in a chronic in vitro model of parkinsonism. Neurotox Res. 2009 Apr;15(3):260-73. Epub 2009 Feb 24. To provide a broader perspective on the parkinsonian neurodegenerative process, we have performed a global analysis of gene expression changes caused by chronic, low-level exposure of neuroblastoma cells to the mitochondrial complex I inhibitor and parkinsonian neurotoxin rotenone. |
32(0,1,1,2) | Details |
17149696 | Dudimah FD, Odman-Ghazi SO, Hatcher F, Whalen MM: Effect of tributyltin (TBT) on ATP levels in human natural killer (NK) cells: relationship to TBT-induced decreases in NK function. J Appl Toxicol. 2007 Jan-Feb;27(1):86-94. In this study NK cells were exposed to various concentrations of TBT and to two other compounds that interfere with ATP synthesis (rotenone a complex I inhibitor and oligomycin an ATP synthase inhibitor) for various lengths of time before determining the levels of ATP and lytic function. |
31(0,1,1,1) | Details |
19924288 | Xiong N, Huang J, Zhang Z, Zhang Z, Xiong J, Liu X, Jia M, Wang F, Chen C, Cao X, Liang Z, Sun S, Lin Z, Wang T: Stereotaxical infusion of rotenone: a reliable rodent model for Parkinson's disease. Mech Ageing Dev. 1997 Nov;98(2):95-111. To overcome these limitations, we developed a rat model by stereotaxically (ST) infusing small doses of the mitochondrial complex-I inhibitor, rotenone, into two brain sites: the right ventral tegmental area and the substantia nigra. |
31(0,1,1,1) | Details |
15384065 | Zhu C, Vourc'h P, Fernagut PO, Fleming SM, Lacan S, Dicarlo CD, Seaman RL, Chesselet MF: Variable effects of chronic subcutaneous administration of rotenone on striatal histology. J Comp Neurol. 2004 Oct 25;478(4):418-26. When infused in rats, rotenone, a mitochondrial complex I inhibitor, induces alterations that resemble the histological changes of Parkinson's disease, particularly degeneration of the nigrostriatal dopaminergic system. |
31(0,1,1,1) | Details |
17646711 | Kim BJ, Jeon JH, Kim SJ, So I, Kim KW: Regulation of transient receptor potential melastatin 7 (TRPM7) currents by mitochondria. J Neurosci Res. 1999 Jul 15;57(2):195-206. The respiratory chain complex I inhibitor, rotenone, and complex III inhibitor, antimycin A, were without effect as were an activator of the mitochondrial Ca2+ uniporter, and ruthenium red, an inhibitor of the mitochondrial Ca2+ uniporter. |
31(0,1,1,1) | Details |
19605638 | Bao L, Avshalumov MV, Patel JC, Lee CR, Miller EW, Chang CJ, Rice ME: Mitochondria are the source of peroxide for dynamic brain-cell signaling. Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):14-24. Using direct fluorescence imaging of H (2) O (2) and tissue analysis of ATP, we found that coapplication of rotenone (50 nM), a mitochondrial complex I inhibitor, and (5 mM), a complex II substrate, limited H (2) O (2) production, but maintained tissue ATP content. |
31(0,1,1,1) | Details |
19874289 | Avila-Gomez IC, Velez-Pardo C, Jimenez-Del-Rio M: Effects of insulin-like growth factor-1 on rotenone-induced apoptosis in human lymphocyte cells. Biochim Biophys Acta. 2006 Dec;1757(12):1568-74. Epub 2006 Sep 29. The present work shows that rotenone, a mitochondrial complex I inhibitor, induced time- and concentration-dependent apoptosis in lymphocytes which was mediated by anion radicals (O (2)*(-))/ peroxide, depolarization of mitochondria, caspase-3 activation, concomitantly with the nuclear translocation of transcription factors such as NF-kappaB, p53, c-Jun and nuclei fragmentation. |
31(0,1,1,1) | Details |
16781463 | Guidarelli A, Sciorati C, Clementi E, Cantoni O: These results, along with our previous findings indicating that the DNA damage induced by is also suppressed by inhibition of the electron flow through complex I, e.g., by rotenone, or by the respiration-deficient phenotype, demonstrate that the mitochondrial formation of DNA-damaging species is critically regulated by the inhibition of complex III and by the availability of Ca (2+). |
mobilizes ions from ryanodine-sensitive stores, a process associated with the mitochondrial accumulation of the cation and the enforced formation of species mediating cleavage of genomic DNA. Neurochem Res. 2003 Oct;28(10):1575-81.31(0,1,1,1) | Details |
12153473 | Poppe M, Reimertz C, Munstermann G, Kogel D, Prehn JH: medulloblastoma cells requires mitochondrial respiratory chain activity but occurs independently of caspases and is not sensitive to Bcl-xL overexpression. Biochem J. 1987 Nov 1;247(3):657-62. Treatment with the complex I inhibitor rotenone, C2- or C8- induced cell death in D283 control cells, while rho- cells were significantly protected. |
-induced apoptosis of D283 31(0,1,1,1) | Details |
12758076 | Marques I, Duarte M, Videira A: The 9.8 kDa subunit of complex I, related to bacterial Na (+)-translocating NADH dehydrogenases, is required for enzyme assembly and function in Neurospora crassa. J Appl Physiol. 2000 Jul;89(1):72-80. Respiration of mutant mitochondria on matrix is rotenone-insensitive, confirming that the 9.8 kDa protein is required for the assembly and activity of complex I. |
8(0,0,1,3) | Details |
8063722 | Majander A, Finel M, Wikstrom M: Diphenyleneiodonium inhibits reduction of iron- clusters in the mitochondrial NADH-ubiquinone oxidoreductase (Complex I). Brain Res Mol Brain Res. 2005 Mar 24;134(1):109-18. Epub 2005 Jan 6. Similar results were found with Complex I and two rotenone-insensitive preparations, subcomplex I lambda and the flavoprotein fraction. |
8(0,0,1,3) | Details |
8307034 | Friedrich T, van Heek P, Leif H, Ohnishi T, Forche E, Kunze B, Jansen R, Trowitzsch-Kienast W, Hofle G, Reichenbach H, et al.: Two binding sites of inhibitors in oxidoreductase (complex I). Anticancer Drugs. 2009 Oct;20(9):770-8. Class II inhibitors including the naturally occurring rotenone, phenoxan, aureothin and the synthetic benzimidazole inhibit complex I from all species in an non-competitive manner, but have no effect on the glucose dehydrogenase. |
4(0,0,0,4) | Details |
17060316 | O'Malley Y, Fink BD, Ross NC, Prisinzano TE, Sivitz WI: Reactive targeted antioxidant administration in endothelial cell mitochondria. J Biol Chem. 2006 Dec 29;281(52):39766-75. Epub 2006 Oct 23. ROS measured by fluorescence resulted from complex I released to the matrix and converted to H (2) O (2). ROS fluorescence by mitochondria fueled by the complex II substrate, was substantial but markedly inhibited by rotenone. |
and 4(0,0,0,4) | Details |
8571432 | Piantadosi CA, Zhang J: Mitochondrial generation of reactive brain ischemia in the rat. J Neurochem. 2005 May;93(3):526-37. was infused into the hippocampus during the experiments, and changes in the recovery of its hydroxylated product, (2,3- were used to assess the effects of inhibitors of mitochondrial complex I on formation of during IR. |
species after 3(0,0,0,3) | Details |
17530440 | Liu Y, Qiao DR, Zheng HB, Dai XL, Bai LH, Zeng J, Cao Y: Cloning and sequence analysis of the gene encoding 19-kD subunit of Complex I from Dunaliella salina. FEMS Yeast Res. 2003 Apr;3(2):141-8. The 19-kD subunit mRNA expression was observed in oxygen deficiency, salt treatment, and rotenone treatment with lower levels. |
3(0,0,0,3) | Details |
18395512 | Lambert AJ, Buckingham JA, Boysen HM, Brand MD: Diphenyleneiodonium acutely inhibits reactive species production by mitochondrial complex I during reverse, but not forward electron transport. Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3436-41. We investigated the effects of diphenyleneiodonium (DPI) on production by complex I in mitochondria isolated from rat skeletal muscle. It had no effect on production during forward electron transport from NAD-linked substrates in the presence of rotenone (to maximise production from the flavin of complex I) or antimycin (to maximise production from complex III), suggesting that the effects of DPI were not through inhibition of the flavin. |
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3456345 | Davies KJ, Doroshow JH: Redox cycling of anthracyclines by cardiac mitochondria. Neurobiol Aging. 2010 Apr;31(4):636-46. Epub 2008 Jul 17. In the present study we have used beef heart submitochondrial preparations (BH-SMP) to demonstrate that a component of mitochondrial Complex I, probably the NADH dehydrogenase flavin, is the mitochondrial site of anthracycline reduction. Inhibitor experiments (rotenone, amytal, piericidin A) indicated that the anthracycline reduction site lies on the substrate side of |
2(0,0,0,2) | Details |
11245784 | Joseph-Horne T, Hollomon DW, Wood PM: Fungal respiration: a fusion of standard and alternative components. FEBS Lett. 2010 Mar 5;584(5):883-8. Epub 2010 Jan 13. These consist of alternative NADH dehydrogenases, which catalyse rotenone insensitive oxidation of matrix or enable cytoplasmic to be used directly. A few fungi lack Complex I. |
2(0,0,0,2) | Details |
17992568 | Ahmadi FA, Grammatopoulos TN, Poczobutt AM, Jones SM, Snell LD, Das M, Zawada WM: neurons to rotenone-induced apoptosis. Neurochem Res. 2008 May;33(5):886-901. Epub 2007 Nov 10. Our results demonstrate that an inhibitor of mitochondrial complex I and increased cytosolic DA may cooperatively lead to conditions of elevated oxidative stress and thereby promote selective demise of dopaminergic neurons. |
selectively sensitizes dopaminergic 1(0,0,0,1) | Details |
3005279 | Doroshow JH, Davies KJ: Redox cycling of anthracyclines by cardiac mitochondria. J Pharmacol Exp Ther. 1997 Feb;280(2):638-49. In the presence of rotenone, initial rates of consumption and formation were identical under comparable experimental conditions. Chem. 261, 3060-3067), we have demonstrated that anthracycline antibiotics are reduced to the semiquinone form at Complex I of the mitochondrial electron transport chain. |
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11724769 | Lee HJ, Shin SY, Choi C, Lee YH, Lee SJ: Formation and removal of alpha-synuclein aggregates in cells exposed to mitochondrial inhibitors. Jpn J Cancer Res. 1992 Aug;83(8):899-906. Treatment with rotenone, an inhibitor of complex I, resulted in an increase of detergent-resistant alpha-synuclein aggregates and a reduction in ATP level. Treatment with rotenone, an inhibitor of complex I, resulted in an increase of detergent-resistant alpha-synuclein aggregates and a reduction in ATP level. |
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16120296 | Setterfield K, Williams AJ, Donald J, Thorburn DR, Kirby DM, Trounce I, Christodoulou J: Flow cytometry in the study of mitochondrial respiratory chain disorders. Biochem Pharmacol. 1993 May 25;45(10):2115-22. Cells were incubated overnight in serum free media, followed by incubation with dihydroethidium with and without rotenone, and then analysed using flow cytometry to measure fluorescence. The change in fluorescence was significantly lower in four of the six patient cell lines, with a correlation between the activity of complex I and change in fluorescence. |
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16029202 | Buchheim K, Wessel O, Siegmund H, Schuchmann S, Meierkord H: Processes and components participating in the generation of intrinsic optical signal changes in vitro. Mitochondrion. 2002 May;1(5):437-45. Rotenone, an inhibitor of mitochondrial complex I, yielded decreased amplitudes of the intrinsic optical signal (27 +/- 7% after 40 min, P < 0.01). Rotenone, an inhibitor of mitochondrial complex I, yielded decreased amplitudes of the intrinsic optical signal (27 +/- 7% after 40 min, P < 0.01). |
1(0,0,0,1) | Details |
8226801 | Ohtsuka T, Nishijima M, Suzuki K, Akamatsu Y: Mitochondrial dysfunction of a cultured Chinese hamster ovary cell mutant deficient in J Cardiovasc Pharmacol. 2000 Nov;36(5 Suppl 1):S205-8. Of the respiratory chain complexes, rotenone-sensitive -ubiquinone reductase (Complex I) was most severely impaired in the mutant, whereas its activity was restored in a revertant of the mutant that had regained the ability to synthesize CL. |
81(1,1,1,1) | Details |
9023274 | Kruidering M, Van de Water B, de Heer E, Mulder GJ, Nagelkerke JF: Cisplatin-induced nephrotoxicity in porcine proximal tubular cells: mitochondrial dysfunction by inhibition of complexes I to IV of the respiratory chain. Carcinogenesis. 1989 May;10(5):913-20. Only N,N'-bis (2-chloroethyl)-N-nitrosourea with rotenone (complex I inhibitor) induced ROS formation, which indicates that inhibition of complex I and inhibition of the GSH-Rd is probably the cause of ROS formation. |
81(1,1,1,1) | Details |
20022987 | Tatpati LL, Irving BA, Tom A, Bigelow ML, Klaus K, Short KR, Nair KS: The effect of branched chain amino acids on skeletal muscle mitochondrial function in young and elderly adults. Neurochem Int. 2007 Mar;50(4):601-6. Epub 2007 Jan 18. Results: In young participants, MAPR with the substrates plus (supplying electrons to complex I) and plus rotenone (complex II) increased in response to BCAA infusion, relative to a decline in MAPR in response to the saline infusion. |
81(1,1,1,1) | Details |
17490603 | Koopman WJ, Hink MA, Verkaart S, Visch HJ, Smeitink JA, Willems PH: Partial complex I inhibition decreases mitochondrial motility and increases matrix protein diffusion as revealed by fluorescence correlation spectroscopy. Neurochem Int. 2008 Feb;52(3):487-94. Epub 2007 Aug 19. We previously reported that inhibition of mitochondrial complex I (CI) by rotenone induces marked increases in mitochondrial length and degree of branching, thus revealing a relationship between mitochondrial function and shape. |
81(1,1,1,1) | Details |
17474759 | Murai M, Ishihara A, Nishioka T, Yagi T, Miyoshi H: The ND1 subunit constructs the inhibitor binding domain in bovine heart mitochondrial complex I. Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H978-H989. Epub 2008 Jun 20. A variety of complex I inhibitors such as piericidin A and rotenone efficiently suppressed the specific binding of [125I] TDA to ND1, indicating that they share a common binding domain. |
38(0,1,1,8) | Details |
18197244 | Marella M, Seo BB, Nakamaru-Ogiso E, Greenamyre JT, Matsuno-Yagi A, Yagi T: Protection by the NDI1 gene against neurodegeneration in a rotenone rat model of Parkinson's disease. FEBS Lett. 1999 May 21;451(2):157-61. In fact, rotenone, a complex I inhibitor, has been used for establishing PD models both in vitro and in vivo. |
38(0,1,2,3) | Details |
17346667 | Sgobbo P, Pacelli C, Grattagliano I, Villani G, Cocco T: Carvedilol inhibits mitochondrial complex I and induces resistance to H2O2 -mediated oxidative insult in H9C2 myocardial cells. Biochem Biophys Res Commun. 2001 Dec 21;289(5):973-8. A similar protective effect on mitochondrial respiration could be obtained by pre-treatment of the cells with a sub-saturating amount of rotenone, a complex I inhibitor. |
34(0,1,1,4) | Details |
10747996 | Scacco S, Vergari R, Scarpulla RC, Technikova-Dobrova Z, Sardanelli A, Lambo R, Lorusso V, Papa S: cAMP-dependent phosphorylation of the nuclear encoded 18-kDa (IP) subunit of respiratory complex I and activation of the complex in serum-starved mouse fibroblast cultures. J Biol Chem. 2000 Jun 9;275(23):17578-82. Phosphorylation of the 18-kDa subunit, in response to cholera toxin treatment of fibroblasts, was accompanied by a 2-3-fold enhancement of the rotenone-sensitive endogenous respiration of fibroblasts, of the rotenone-sensitive oxidase, and of the NADH:ubiquinone oxidoreductase activity of complex I. |
34(0,1,1,4) | Details |
17084831 | Shinde SB, Save VC, Patil ND, Mishra KP, Tendolkar AG: Impairment of mitochondrial respiratory chain enzyme activities in tetralogy of Fallot. Clin Chim Acta. 2007 Feb;377(1-2):138-43. Epub 2006 Sep 26. The activities of rotenone-sensitive cytochrome c reductase (complexes I+III), cytochrome c oxidase (complex IV) and the ratio of I and III to II and III complexes (complex I) were significantly lower in TOF (p <0.001). |
32(0,1,1,2) | Details |
17855661 | Hsu YC, Lee HC, Ping YH, Liu TY, Lui WY, Chi CW: Mitochondria are an essential mediator of /cyclic 3',5'-monophosphate blocking of depletion induced cytotoxicity in human HepG2 cells. Mol Biochem Parasitol. 1991 Apr;45(2):185-92. Furthermore, we found that rotenone and antimycin A (mitochondria complex I and III inhibitors, respectively) blocked SNP cytoprotection against depletion-induced cytotoxicity. |
32(0,1,1,2) | Details |
11971654 | Krungkrai J, Kanchanarithisak R, Krungkrai SR, Rochanakij S: Mitochondrial NADH dehydrogenase from Plasmodium falciparum and Plasmodium berghei. J Mol Biol. 2002 Jun 21;319(5):1211-21. NADH dehydrogenase of respiratory complex I was demonstrated in isolated mitochondrial organelles of the human parasite Plasmodium falciparum and the mouse parasite Plasmodium berghei by using the specific inhibitor rotenone on consumption and enzyme activity. |
32(0,1,1,2) | Details |
19074024 | Rojas JC, Lee J, John JM, Gonzalez-Lima F: Neuroprotective effects of near-infrared light in an in vivo model of mitochondrial optic neuropathy. J Neurosci. 1996 Jun 15;16(12):3807-16. Subjects were pigmented rats that received single bilateral intravitreal doses of rotenone, a mitochondrial complex I inhibitor, or rotenone plus one of three different doses of NIL. |
32(0,1,1,2) | Details |
19114014 | Borland MK, Trimmer PA, Rubinstein JD, Keeney PM, Mohanakumar K, Liu L, Bennett JP Jr: Chronic, low-dose rotenone reproduces Lewy neurites found in early stages of Parkinson's disease, reduces mitochondrial movement and slowly kills differentiated SH-SY5Y neural cells. Bioorg Med Chem. 2010 Feb;18(3):1312-20. Epub 2009 Dec 26. RESULTS: We developed a differentiation protocol for human SH-SY5Y neuroblastoma that yielded non-dividing dopaminergic neural cells with long processes that we then exposed to 50 nM rotenone, a complex I inhibitor used in Parkinson's disease models. |
32(0,1,1,2) | Details |
15371739 | Isaev NK, Stelmashook EV, Ruscher K, Andreeva NA, Zorov DB: reduces rotenone-induced cell death in cerebellar granule neurons. Life Sci. 2003 Nov 7;73(25):3277-88. Chemical hypoxia (term defining the simulation by using respiratory inhibitors) chosen as in vitro ischemic model, was induced in primary cultures of rat cerebellar granule neurons by inhibitors of mitochondrial electron transport such as rotenone or paraquat (complex I), 3-nitropropionic acid (3-NPA, complex II), antimycin A (complex III), or azide (complex IV). |
31(0,1,1,1) | Details |
8790427 | Murphy AN, Bredesen DE, Cortopassi G, Wang E, Fiskum G: Bcl-2 potentiates the maximal uptake capacity of neural cell mitochondria. Biochem J. 1977 Aug 1;165(2):295-301. This difference was less apparent when respiration was driven by the oxidation of in the presence of the respiratory complex I inhibitor rotenone. |
31(0,1,1,1) | Details |
12603842 | Tai KK, McCrossan ZA, Abbott GW: Activation of mitochondrial ATP-sensitive channels increases cell viability against rotenone-induced cell death. J Mol Biol. 2003 May 30;329(2):283-90. We recently showed that activation of ATP-sensitive (KATP) channels in PC12 cells induces protection against the effect of rotenone, a mitochondrial complex I inhibitor. |
31(0,1,1,1) | Details |
16342116 | Koopman WJ, Visch HJ, Smeitink JA, Willems PH: Simultaneous quantitative measurement and automated analysis of mitochondrial morphology, mass, potential, and motility in living human skin fibroblasts. Free Radic Res. 2002 Apr;36(4):421-7. It was found that acute inhibition of mitochondrial complex I (NADH:ubiquinone oxidoreductase) by means of rotenone transiently reduced mitochondrial branching, area, and potential. |
31(0,1,1,1) | Details |
15964900 | Chapman KE, Sinclair SE, Zhuang D, Hassid A, Desai LP, Waters CM: Cyclic mechanical strain increases reactive production in pulmonary epithelial cells. Biochim Biophys Acta. 2001 Apr 2;1504(2-3):173-8. Rotenone, a mitochondrial complex I inhibitor, partially abrogated the stretch-induced generation of O2- after 2 h CMS in 16HBE cells. |
species 31(0,1,1,1) | Details |
16663636 | Ravanel P, Tissut M, Douce R: Effects of Rotenoids on Isolated Plant Mitochondria. . Am J Physiol Lung Cell Mol Physiol. 2005 Nov;289(5):L834-41. Epub 2005 Jun 17. Then, a one-third decrease of the ADP/O ratio can be measured.Such a selective inhibition of complex I is obtained with deguelin, tephrosin, elliptone, OH-12 rotenone, and almost all the rotenoids extracted from Derris roots. |
31(0,1,1,1) | Details |
8981035 | Rao DN, Cederbaum AI: A comparative study of the redox-cycling of a (rifamycin S) and a quinonimine (rifabutin) antibiotic by rat liver microsomes. J Biol Chem. 2001 Mar 23;276(12):9038-44. Epub 2000 Dec 21. The electron transport chain inhibitors such as rotenone and antimycin A enhanced the signal intensity of DMPO-OH, suggesting NADH dehydrogenase (complex I) as the major component involved in the reduction of rifamycin S. |
31(0,1,1,1) | Details |
17881465 | Ding G, Zhang A, Huang S, Pan X, Zhen G, Chen R, Yang T: ANG II induces c-Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR. Biochem Pharmacol. 1988 Jul 1;37(13):2551-8. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex I inhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P-450 oxygenase inhibitor ketoconazole, and the synthase inhibitor N (G)-nitro- methyl ester, were without effect. |
31(0,1,1,1) | Details |
15254374 | Herrero A, Barja G: Localization of the site of complex I of heart and nonsynaptic brain mammalian mitochondria. Pediatr Neurol. 1998 Oct;19(4):308-12. The results, taking together, show that rotenone stimulates -supported generation, confirming that complex I is a source of radicals in mammals, in general. |
radical generation inside the 8(0,0,1,3) | Details |
10924899 | Zickermann V, Kurki S, Kervinen M, Hassinen I, Finel M: The oxidation domain of complex I: do bacterial and mitochondrial enzymes catalyze ferricyanide reduction similarly?. Biochim Biophys Acta. 2000 Jul 20;1459(1):61-8. |
7(0,0,0,7) | Details |
17017541 | Schmidt WJ, Alam M: Controversies on new animal models of Parkinson's disease pro and con: the rotenone model of Parkinson's disease (PD). J Bioenerg Biomembr. 2001 Jun;33(3):233-42. These results support the hypothesis of an involvement of complex I in PD and render the rotenone model as a suitable experimental model. |
7(0,0,1,2) | Details |
14665431 | Feldkamp T, Kribben A, Roeser NF, Senter RA, Kemner S, Venkatachalam MA, Nissim I, Weinberg JM: Preservation of complex I function during hypoxia-reoxygenation-induced mitochondrial injury in proximal tubules. J Neurochem. 2003 Oct;87(2):448-60. During titration of complex I activity with rotenone, progressive reduction of NAD+ to was detected at > 20% complex I inhibition, but substantial decreases in ATP levels and mitochondrial membrane potential did not occur until > 70% inhibition. |
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17055488 | Seo BB, Marella M, Yagi T, Matsuno-Yagi A: The single subunit NADH dehydrogenase reduces generation of reactive species from complex I. FEBS Lett. 2006 Nov 13;580(26):6105-8. Epub 2006 Oct 16. Incubation of non-transduced cells with rotenone elicited oxidative damage to mitochondrial DNA as well as lipid peroxidation. |
4(0,0,0,4) | Details |
10072046 | Carelli V, Ghelli A, Bucchi L, Montagna P, De Negri A, Leuzzi V, Carducci C, Lenaz G, Lugaresi E, Degli Esposti M: Biochemical features of mtDNA 14484 (ND6/M64V) point mutation associated with Leber's hereditary optic neuropathy. Neurochem Int. 2000 May;36(6):489-97. We report the effect on complex I function of the 14484 Leber's hereditary optic neuropathy (LHON) mutation affecting the ND6 subunit gene. |
3(0,0,0,3) | Details |
11695186 | Schuler F, Casida JE: The insecticide target in the PSST subunit of complex I. . Mol Cell Biochem. 1997 Sep;174(1-2):329-33. |
3(0,0,0,3) | Details |
16641458 | Biagini GA, Viriyavejakul P, O'neill PM, Bray PG, Ward SA: Functional characterization and target validation of alternative complex I of Plasmodium falciparum mitochondria. Am J Physiol. 1981 Feb;240(2):H308-13. The inhibitory profile of PfNDH2 revealed that the enzyme activity was insensitive to rotenone, consistent with recent genomic data indicating the absence of the canonical NADH:dehydrogenase enzyme. |
3(0,0,0,3) | Details |
9107311 | Darrouzet E, Dupuis A: Genetic evidence for the existence of two inhibitor binding sites in - reductase. Ann Neurol. 2004 Nov;56(5):631-41. Using the - reductase of Rhodobacter capsulatus as a model for the mitochondrial Complex I, we have for the first time isolated bacterial mutants resistant to piericidin-A, a classical inhibitor of the mitochondrial enzyme. |
related 2(0,0,0,2) | Details |
16679036 | Lopez-Armada MJ, Carames B, Martin MA, Cillero-Pastor B, Lires-Dean M, Fuentes-Boquete I, Arenas J, Blanco FJ: Mitochondrial activity is modulated by TNFalpha and IL-1beta in normal human chondrocyte cells. Biochim Biophys Acta. 1997 Mar 28;1319(1):1-4. Rotenone, an inhibitor of complex I, caused a significant reduction of the red/green ratio, but it did not reduce the viability of the chondrocytes. RESULTS: Compared to basal cells, stimulation with TNFalpha (10 ng/ml) and IL-1beta (5 ng/ml) for 48 h significantly decreased the activity of complex I (TNFalpha=35% and IL-1beta=35%) and the production of ATP (TNFalpha=18% and IL-1beta=19%). |
2(0,0,0,2) | Details |
17657281 | Panee J, Liu W, Nakamura K, Berry MJ: The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of supplementation. J Neurochem. 2003 Feb;84(3):491-502. In summary, our results showed that complex I was the major ROS-generating site in HT22 cells. |
2(0,0,0,2) | Details |
9241135 | Hasegawa E, Kang D, Sakamoto K, Mitsumoto A, Nagano T, Minakami S, Takeshige K: A Dual Effect of 1-Methyl-4-phenylpyridinium (MPP+ )-Analogs on the Respiratory Chain of Bovine Heart Mitochondria. Arch Biochem Biophys. 1997 Jan 1;337(1):69-74. The production of (O- 2 ) induced by MPP+ or analog 8 was to the same extent as that by rotenone, an inhibitor of complex I of the mitochondrial respiratory chain. The production of (O- 2 ) induced by MPP+ or analog 8 was to the same extent as that by rotenone, an inhibitor of complex I of the mitochondrial respiratory chain. |
1(0,0,0,1) | Details |
10433094 | Myers MA, Georgiou HM, Byron S, Esposti MD: Inhibition of mitochondrial oxidative phosphorylation induces hyper-expression of glutamic acid decarboxylase in pancreatic islet cells. Am J Respir Crit Care Med. 2008 Jul 15;178(2):168-79. Epub 2008 Apr 24. Inhibitors of NADH-ubiquinone oxidoreductase (complex I) seem to be particularly effective in increasing the expression of GAD in both foetal mouse pancreas and HIT-T15 hamster beta cells, especially in the presence of nutrients such as and |
1(0,0,0,1) | Details |
16087473 | Saborido A, Soblechero L, Megias A: Isolated respiring heart mitochondria release reactive species in states 4 and 3. Free Radic Res. 2005 Sep;39(9):921-31. As protein concentration was raised in in vitro assays at 37 degrees C, the rate of H2O2 release by rat heart mitochondria supplemented with / or with (plus rotenone) was shown to increase (0.03-0.15 mg protein/ml), to decrease (0.2-0.5 mg protein/ml) and to be negligible (over 0.5 mg protein/ml). Consequently, these findings indicate that isolated mitochondria, respiring in vitro under conditions of forward electron transport, release ROS with Complex I- and II-linked substrates in the resting condition (state 4) and when energy demand is maximal (state 3), provided that there is sufficient dissolved in the medium. |
1(0,0,0,1) | Details |
10878378 | Chandel NS, Trzyna WC, McClintock DS, Schumacker PT: Role of oxidants in NF-kappa B activation and TNF-alpha gene transcription induced by hypoxia and endotoxin. J Immunol. 2000 Jul 15;165(2):1013-21. Rotenone, an inhibitor of mitochondrial complex I, abolished the increase in ROS signal, the activation of NF-kappa B, and TNF-alpha gene transcription during hypoxia. Rotenone, an inhibitor of mitochondrial complex I, abolished the increase in ROS signal, the activation of NF-kappa B, and TNF-alpha gene transcription during hypoxia. |
1(0,0,0,1) | Details |
14511122 | Gyulkhandanyan AV, Feeney CJ, Pennefather PS: Modulation of mitochondrial membrane potential and reactive species production by in astrocytes. Antimicrob Agents Chemother. 2008 Jan;52(1):164-70. Epub 2007 Oct 22. sensitized astrocytes to the action of an intracellular generator of radical, exogenous peroxide (H2O2) and rotenone, an inhibitor of mitochondrial electron transport chain complex I. sensitized astrocytes to the action of an intracellular generator of radical, exogenous peroxide (H2O2) and rotenone, an inhibitor of mitochondrial electron transport chain complex I. |
1(0,0,0,1) | Details |
2590688 | Sled' VD, Zinich VN, Kotliar AB: [One- and two-electron reduction of homologs by - dehydrogenase preparations from the mitochondrial respiratory chain]. J Neurosci. 2009 Sep 9;29(36):11257-62. The mechanism of homologs reduction by different preparations of mitochondrial NADH dehydrogenase: complex I within submitochondrial particles, isolated NADH-ubiquinone oxidoreductase and soluble low molecular weight NADH dehydrogenase, has been investigated. It has been shown that oxidation via the rotenone-insensitive reaction is associated with one-electron reduction of low molecular weight homologs (Q0, Q1, Q2) to semiquinone with subsequent fast oxidation of the latter by atmospheric to form a |
1(0,0,0,1) | Details |
18242195 | Del Prete A, Zaccagnino P, Di Paola M, Saltarella M, Oliveros Celis C, Nico B, Santoro G, Lorusso M: Role of mitochondria and reactive species in dendritic cell differentiation and functions. Neurobiol Dis. 2009 May;34(2):357-65. Epub 2009 Feb 20. The presence in the culture medium of rotenone, an inhibitor of the respiratory chain Complex I, prevented the increase in mitochondrial number and ATP level, without affecting cell viability. The presence in the culture medium of rotenone, an inhibitor of the respiratory chain Complex I, prevented the increase in mitochondrial number and ATP level, without affecting cell viability. |
1(0,0,0,1) | Details |
18836818 | Kumar B, Kumar A, Pandey BN, Mishra KP, Hazra B: Role of mitochondrial oxidative stress in the apoptosis induced by diospyrin diethylether in human breast carcinoma (MCF-7) cells. Mol Cell Biochem. 2009 Jan;320(1-2):185-95. Epub 2008 Oct 4. Experiments using suitable inhibitors also demonstrated that D7 could alter the electron flow in mitochondrial electron transport chain by affecting target (s) between complex I and complex III, and indicated the probable site of D7-induced generation of ROS. |
1(0,0,0,1) | Details |
10904037 | Nethery D, Callahan LA, Stofan D, Mattera R, DiMarco A, Supinski G: PLA (2) dependence of diaphragm mitochondrial formation of reactive species. Biochim Biophys Acta. 2009 May;1787(5):384-92. Epub 2008 Nov 14. We also found that administration of (the principal metabolic product of PLA (2) activation) increased mitochondrial H (2) O (2) formation by interacting with complex I of the electron transport chain. |
1(0,0,0,1) | Details |
16579629 | Mirzaei H, Schieler JL, Rochet JC, Regnier F: Identification of rotenone-induced modifications in alpha-synuclein using affinity pull-down and tandem mass spectrometry. Exp Neurol. 2007 Nov;208(1):120-6. Epub 2007 Aug 22. Using this method, we mapped posttranslational modifications of alpha-synuclein from untreated neurons and neurons exposed to rotenone, an inhibitor of mitochondrial complex I. |
1(0,0,0,1) | Details |
12632423 | Maneiro E, Martin MA, de Andres MC, Lopez-Armada MJ, Fernandez-Sueiro JL, del Hoyo P, Galdo F, Arenas J, Blanco FJ: Mitochondrial respiratory activity is altered in osteoarthritic human articular chondrocytes. Arch Biochem Biophys. 1999 Sep 1;369(1):119-26. The activities of mitochondrial respiratory chain complexes (complex I: rotenone-sensitive - (1) reductase; complex II: succinate dehydrogenase; complex III: antimycin-sensitive ubiquinol cytochrome c reductase; and complex IV: cytochrome c oxidase) and CS were measured in human articular chondrocytes isolated from OA and normal cartilage. |
81(1,1,1,1) | Details |
18850458 | Hayworth CR, Rojas JC, Gonzalez-Lima F: Transgenic mice expressing cyan fluorescent protein as a reporter strain to detect the effects of rotenone toxicity on retinal ganglion cells. Exp Neurol. 2010 Jan;221(1):217-24. Epub 2009 Nov 11. Rotenone is a widely used pesticide that inhibits mitochondrial complex I and produces neurotoxicity. |
81(1,1,1,1) | Details |
12867501 | Gao HM, Liu B, Hong JS: Critical role for microglial rotenone-induced degeneration of dopaminergic neurons. Biochim Biophys Acta. 2010 Mar;1800(3):275-81. Epub 2009 Sep 23. Mechanistically, rotenone-induced dopaminergic neurodegeneration has been associated with both its inhibition of neuronal mitochondrial complex I and the enhancement of activated microglia. |
oxidase in 81(1,1,1,1) | Details |
11225736 | Li YP, Atkins CM, Sweatt JD, Reid MB: Mitochondria mediate tumor necrosis factor-alpha/NF-kappaB signaling in skeletal muscle myotubes. Biochem Int. 1986 Aug;13(2):351-7. We found that activation of NF-kappaB by TNF-alpha was blocked by rotenone or amytal, inhibitors of complex I of the mitochondrial respiratory chain. |
81(1,1,1,1) | Details |
16402917 | Reinecke F, Levanets O, Olivier Y, Louw R, Semete B, Grobler A, Hidalgo J, Smeitink J, Olckers A, Van der Westhuizen FH: Metallothionein isoform 2A expression is inducible and protects against ROS-mediated cell death in rotenone-treated HeLa cells. J Hypertens. 2006 Apr;24(4):757-66. HeLa cells were titrated with rotenone, resulting in dose-dependent decrease in complex I activity and elevated ROS production at activities lower than 33%. |
38(0,1,2,3) | Details |
9593947 | Lummen P: Complex I inhibitors as insecticides and acaricides. Biochem Pharmacol. 1991 Mar 1;41(5):677-84. Mechanistic studies indicated that these compounds interfered with reduction most likely at the same site (s) as the classical complex I inhibitors rotenone and piericidin A. |
37(0,1,1,7) | Details |
16887699 | Woznica A, Dzirba J, Manka D, Labuzek S: Effects of electron transport inhibitors on iron reduction in Aeromonas hydrophila strain KB1. Anaerobe. 2003 Jun;9(3):125-30. The observed inhibition of iron reduction by rotenone and may suggest the existence of Q sites in reductase, analogous to those in complex I. |
37(0,1,2,2) | Details |
9824162 | Higuchi M, Proske RJ, Yeh ET: Inhibition of mitochondrial respiratory chain complex I by TNF results in cytochrome c release, membrane permeability transition, and apoptosis. Life Sci. 2006 May 15;78(25):2889-97. Epub 2005 Dec 27. This hypothesis is supported by the following observations: (1) TNF and rotenone induced MPT and cytochrome c release; (2) TNF-induced complex I inhibition was observed prior to cytochrome c release and MPT induction; (3) MPT induction was inhibited by a caspase 3 inhibitor, z-DEVD-CH2F, and an antioxidant pyrrolidine dithiocarbamate (PDTC), whereas cytochrome c release was only inhibited by PDTC. |
35(0,1,1,5) | Details |
1959619 | Majander A, Huoponen K, Savontaus ML, Nikoskelainen E, Wikstrom M: Electron transfer properties of NADH:ubiquinone reductase in the ND1/3460 and the ND4/11778 mutations of the Leber hereditary optic neuroretinopathy (LHON). Arch Biochem Biophys. 1992 Sep;297(2):253-7. The ND1/3460 mutation exhibits 80% reduction in rotenone-sensitive and -dependent electron transfer activity, whereas the proximal NADH dehydrogenase activity of the Complex is unaffected. |
34(0,1,1,4) | Details |
9449419 | Seaton TA, Cooper JM, Schapira AH: Free radical scavengers protect dopaminergic cell lines from apoptosis induced by complex I inhibitors. Biochemistry. 1992 Nov 24;31(46):11413-9. We have demonstrated that complex I inhibitors, including rotenone, MPP+, isoquinoline and tetrahydroisoquinoline, induce apoptosis in PC12 and SK-N-MC dopaminergic cell lines which was decreased by pretreatment with TEMPO, dihydrolipoic acid or pyrrolidine dithiocarbamate. |
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12558969 | Hoglinger GU, Feger J, Prigent A, Michel PP, Parain K, Champy P, Ruberg M, Oertel WH, Hirsch EC: Chronic systemic complex I inhibition induces a hypokinetic multisystem degeneration in rats. Mol Carcinog. 2010 Feb;49(2):141-51. Male Lewis rats infused with rotenone, a lipophilic complex I inhibitor [2.5 mg/kg/day intraveneously (i.v.) for 28 days], were compared with vehicle-infused controls. |
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7945357 | Sivan VM, Raj RK: Lactate oxidation coupled to energy production in mitochondria like particles from Setaria digitata, a filarial parasite. Biochem Biophys Res Commun. 1994 Oct 14;204(1):17-22. The ferricyanide reduction by lactate is found to be sensitive to the cytochrome o inhibitor orthohydroxy diphenyl (OHD) and complex I inhibitor rotenone, modulated by ADP (+) and ATP (-) and inhibited by and |
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12062197 | Agani FH, Pichiule P, Carlos Chavez J, LaManna JC: Inhibitors of mitochondrial complex I attenuate the accumulation of hypoxia-inducible factor-1 during hypoxia in Hep3B cells. Invest Ophthalmol Vis Sci. 2003 Mar;44(3):1312-9. Because mitochondria have been postulated to be involved in the regulation of HIF-1, we tested the effects of mitochondrial electron transport chain complex I inhibitors, rotenone and 1-methyl-4-phenylpiridinium (MPP (+)), on hypoxic-induced accumulation of HIF-1 alpha, the regulated component of the dimer. |
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15590775 | Melo AM, Bandeiras TM, Teixeira M: New insights into type II NAD (P) H:quinone oxidoreductases. Biochim Biophys Acta. 2006 May-Jun;1757(5-6):525-34. Epub 2006 Apr 7. However, they have the common feature of being resistant to the complex I classical inhibitors rotenone, and piericidin A. |
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1787040 | Mendis AH, Armson A, Thompson RC, Grubb WB: The response of intact Strongyloides ratti infective (L3) larvae to substrates and inhibitors of respiratory electron transport. Microbiol Mol Biol Rev. 2004 Dec;68(4):603-16. Respiratory electron transport (RET) Complex I inhibitor rotenone (2 microM) produced 33 +/- 6.5% inhibition of the E-QO2. |
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6745260 | Cook ND, Cammack R: Purification and characterization of the rotenone-insensitive NADH dehydrogenase of mitochondria from Arum maculatum. Biochem Mol Med. 1996 Dec;59(2):134-7. Affinity chromatography on 5'-ADP-Sepharose 4B was used to separate the rotenone-sensitive (complex I) NADH dehydrogenase from the rotenone-insensitive NADH dehydrogenase. |
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11198300 | Lotharius J, O'Malley KL: Role of mitochondrial dysfunction and amphetamine-induced toxicity. Ann Neurol. 2001 Jan;49(1):79-89. In contrast, when primary cultures of dopaminergic neurons were exposed to AMPH in the presence of subtoxic doses of the mitochondrial complex I inhibitor rotenone, cell death was dramatically increased, mimicking the effects of a known parkinsonism-inducing toxin. |
-dependent oxidative stress in 31(0,1,1,1) | Details |
15223368 | Kanki R, Nakamizo T, Yamashita H, Kihara T, Sawada H, Uemura K, Kawamata J, Shibasaki H, Akaike A, Shimohama S: Effects of mitochondrial dysfunction on glutamate receptor-mediated neurotoxicity in cultured rat spinal motor neurons. Cytometry A. 2006 Jan;69(1):1-12. We investigated the relationship between excitotoxicity and mitochondrial dysfunction elicited by rotenone (a complex I inhibitor), (a complex II inhibitor), or antimycin (a complex III inhibitor), in primary cultures of the embryonic rat spinal cord. |
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7999034 | Pecci L, Fontana M, Montefoschi G, Cavallini D: Aminoethylcysteine ketimine decarboxylated dimer protects submitochondrial particles from lipid peroxidation at a concentration not inhibitory of electron transport. Mol Cell Endocrinol. 2000 Oct 25;168(1-2):127-34. Furthermore the dimer is able to counteract the malondialdehyde formation stimulated by the Complex I inhibitors rotenone and N-methyl-4-phenylpyridinium (MPP+). |
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7959172 | Rembish SJ, Trush MA: Further evidence that lucigenin-derived chemiluminescence monitors mitochondrial macrophages. Am J Physiol Renal Physiol. 2007 Dec;293(6):F1889-97. Epub 2007 Sep 19. The agents examined included a Complex I inhibitor, rotenone; a Complex III inhibitor, antimycin a; and a Complex IV inhibitor, KCN. |
generation in rat alveolar 31(0,1,1,1) | Details |
19384599 | Rojas JC, John JM, Lee J, Gonzalez-Lima F: Methylene blue provides behavioral and metabolic neuroprotection against optic neuropathy. Neuroreport. 2002 Jul 19;13(10):1279-83. Methylene blue (MB) is a diaminophenothiazine with potent antioxidant and unique redox properties that prevent morphologic degenerative changes in the mouse retina induced by rotenone, a specific mitochondrial complex I inhibitor. |
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17123556 | Leung KW, Yung KK, Mak NK, Chan YS, Fan TP, Wong RN: Neuroprotective effects of ginsenoside-Rg1 in primary nigral neurons against rotenone toxicity. Biochem Biophys Res Commun. 1993 Oct 15;196(1):355-62. Rotenone, a common household pesticide known for its specific and irreversible mitochondria complex I inhibition, has been suggested to be the causal agent of Parkinson's disease (PD) by inducing degeneration of cells in the substantial nigra. |
31(0,1,1,1) | Details |
9915790 | Okun JG, Lummen P, Brandt U: Three classes of inhibitors share a common binding domain in mitochondrial complex I (NADH:ubiquinone oxidoreductase). J Physiol. 1997 Oct 1;504 ( Pt 1):175-89. Although the rotenone site overlaps with both the piericidin A and the site, the latter two sites do not overlap. |
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3178753 | Cottingham IR, Moore AL: Analysis of NADH dehydrogenases from plant [mung bean (Phaseolus aureus)] mitochondrial membranes on non-denaturing polyacrylamide gels and purification of complex I by band excision. Biochemistry. 1994 Aug 16;33(32):9675-83. A rotenone-sensitive NADH dehydrogenase (Complex I) was identified on the basis of co-migration with the purified mammalian enzyme. |
7(0,0,1,2) | Details |
12566073 | Fang J, Beattie DS: External alternative NADH dehydrogenase of Saccharomyces cerevisiae: a potential source of Biochem J. 1979 Apr 15;180(1):129-35. Three rotenone-insensitive NADH dehydrogenases are present in the mitochondria of yeast Saccharomyces cerevisiae, which lack complex I. |
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18486594 | Fendel U, Tocilescu MA, Kerscher S, Brandt U: Exploring the inhibitor binding pocket of respiratory complex I. . Biochem Biophys Res Commun. 1994 Mar 15;199(2):755-60. Many mutations around the domain of the 49-kDa subunit that is homologous to the [NiFe] centre binding region of hydrogenase conferred resistance to DQA (class I/type A) and rotenone (class II/type B) indicating a wider overlap of the binding sites for these two types of inhibitors. |
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8439309 | Degli Esposti M, Ghelli A, Crimi M, Estornell E, Fato R, Lenaz G: Complex I and complex III of mitochondria have common inhibitors acting as antagonists. Histochem J. 2000 Mar;32(3):133-7. The stigmatellin analog is more powerful than its parent compound and is noncompetitive with exogenous ubiquinones, rotenone and piericidin. |
4(0,0,0,4) | Details |
8068645 | Ahmed I, Krishnamoorthy G: Probing of coenzyme binding site of mitochondrial NADH:CoQ reductase by fluorescence dynamics. Neurochem Int. 2000 May;36(6):483-8. The coenzyme binding region of mitochondrial NADH:CoQ reductase (complex-I) was investigated by the fluorescent probes erythrosine-5'-iodoacetamide (ER) and 3,3'-diethyloxadicarbocyanine iodide (DODCI). Binding of the probes was not affected by the binding of the inhibitor rotenone. |
4(0,0,0,4) | Details |
9795106 | Seaton TA, Cooper JM, Schapira AH: Cyclosporin inhibition of apoptosis induced by mitochondrial complex I toxins. Exp Neurol. 2009 Jul;218(1):154-61. Epub 2009 May 3. The present study using propidium iodide and FITC-TUNEL staining to identify apoptotic cells, demonstrates that rotenone, MPP+ and tetrahydroisoquinoline induce apoptosis in PC12 cells. |
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9030267 | Glinn MA, Lee CP, Ernster L: Pro- and anti-oxidant activities of the mitochondrial respiratory chain: factors influencing NAD (P) H-induced lipid peroxidation. J Biol Chem. 1998 Jun 5;273(23):14210-7. This paper is a study of factors influencing the rate of lipid peroxidation in beef heart submitochondrial particles induced by NAD (P) H via the NADH-ubiquinone oxidoreductase (Complex I) of the respiratory chain. Rotenone did not eliminate the biphasicity of the -induced reaction, indicating that this was not due to an antioxidant effect of at high concentrations. |
3(0,0,0,3) | Details |
17263793 | Tretter L, Takacs K, Hegedus V, Adam-Vizi V: Characteristics of brain mitochondria. Biochemistry. 1998 Aug 25;37(34):11792-6. H (2) O (2) formation and the increase in NAD (P) H level were inhibited by rotenone, ADP or FCCP, respectively, being consistent with a reverse electron transfer (RET). We suggest that the metabolism of alpha-GP leads to ROS generation primarily by complex I in RET, and in addition a significant ROS formation could be ascribed to alpha-GP-dehydrogenase in mammalian brain mitochondria. |
-evoked H2O2 generation in 2(0,0,0,2) | Details |
8630091 | McNaught KS, Thull U, Carrupt PA, Altomare C, Cellamare S, Carotti A, Testa B, Jenner P, Marsden CD: Effects of isoquinoline derivatives structurally related to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on mitochondrial respiration. Brain Res. 2001 Feb 9;891(1-2):94-105. Isoquinoline derivatives exert 1-methyl-4-phenylpyridinium (MPP+)-like activity as inhibitors of complex I and alpha-ketoglutarate dehydrogenase activity in rat brain mitochondrial fragments. None of the compounds examined inhibited respiration supported by either + rotenone or tetramethylparaphenylenediamine (TMPD) + |
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12556227 | Duarte M, Peters M, Schulte U, Videira A: The internal alternative NADH dehydrogenase of Neurospora crassa mitochondria. Toxicology. 2005 Dec;216(1):9-14. Epub 2005 Aug 22. The respiratory activity of mitochondria from the resulting null-mutant ndi1 is almost fully inhibited by rotenone, an inhibitor of the -pumping complex I, when matrix-generated is used as substrate. The respiratory activity of mitochondria from the resulting null-mutant ndi1 is almost fully inhibited by rotenone, an inhibitor of the -pumping complex I, when matrix-generated is used as substrate. |
2(0,0,0,2) | Details |
9395404 | Hasegawa E, Kang D, Sakamoto K, Mitsumoto A, Nagano T, Minakami S, Takeshige K: A dual effect of 1-methyl-4-phenylpyridinium (MPP+)-analogs on the respiratory chain of bovine heart mitochondria. Exp Brain Res. 2007 Aug;181(3):435-46. Epub 2007 Apr 12. The production of (O2-) induced by MPP+ or analog 8 was to the same extent as that by rotenone, an inhibitor of complex I of the mitochondrial respiratory chain. The production of (O2-) induced by MPP+ or analog 8 was to the same extent as that by rotenone, an inhibitor of complex I of the mitochondrial respiratory chain. |
1(0,0,0,1) | Details |
19763263 | Johnson F, Kaplitt MG: Novel mitochondrial substrates of omi indicate a new regulatory role in neurodegenerative disorders. Biochem J. 2006 Dec 15;400(3):541-50. Additionally our gene expression studies, using rotenone (an inhibitor of Complex I) showed Omi expression was silenced when pdhb and idh3a were increased when a sub-lethal dose was applied. Additionally our gene expression studies, using rotenone (an inhibitor of Complex I) showed Omi expression was silenced when pdhb and idh3a were increased when a sub-lethal dose was applied. |
1(0,0,0,1) | Details |
19492085 | Sandebring A, Thomas KJ, Beilina A, van der Brug M, Cleland MM, Ahmad R, Miller DW, Zambrano I, Cowburn RF, Behbahani H, Cedazo-Minguez A, Cookson MR: Mitochondrial alterations in PINK1 deficient cells are influenced by calcineurin-dependent dephosphorylation of dynamin-related protein 1. Biochem Pharmacol. 1993 Feb 9;45(3):691-6. As in previous studies, PINK1 deficient cells have lower mitochondrial membrane potential and are more sensitive to the toxic effects of mitochondrial complex I inhibitors. We also show that wild-type PINK1, but not recessive mutant or kinase dead versions, protects against rotenone-induced mitochondrial fragmentation whereas PINK1 deficient cells show lower mitochondrial connectivity. |
1(0,0,0,1) | Details |
7670095 | Macho A, Castedo M, Marchetti P, Aguilar JJ, Decaudin D, Zamzami N, Girard PM, Uriel J, Kroemer G: Mitochondrial dysfunctions in circulating T lymphocytes from human immunodeficiency virus-1 carriers. Parasitol Res. 2004 Mar;92(4):341-6. Epub 2004 Jan 16. Control experiments involving rotenone, an inhibitor of the respiratory chain complex I, indicate that the reactive species responsible for HE --> Eth conversion is generated during mitochondrial electron transport. Control experiments involving rotenone, an inhibitor of the respiratory chain complex I, indicate that the reactive species responsible for HE --> Eth conversion is generated during mitochondrial electron transport. |
1(0,0,0,1) | Details |
11479321 | Bai Y, Hajek P, Chomyn A, Chan E, Seo BB, Matsuno-Yagi A, Yagi T, Attardi G: Lack of complex I activity in human cells carrying a mutation in MtDNA-encoded ND4 subunit is corrected by the Saccharomyces cerevisiae -quinone oxidoreductase (NDI1) gene. Physiol Behav. 2004 Dec 15;83(3):395-400. The gene for the single subunit, rotenone-insensitive, and -sensitive internal -quinone oxidoreductase of Saccharomyces cerevisiae (NDI1) can completely restore the NADH dehydrogenase activity in mutant human cells that lack the essential mitochondrial DNA (mtDNA)-encoded subunit ND4. |
1(0,0,0,1) | Details |
9417880 | Guidarelli A, Brambilla L, Clementi E, Sciorati C, Cantoni O: Stimulation of linked to, enhanced formation of tert-butylhydroperoxide-induced DNA single-strand breaks. Exp Cell Res. 1997 Nov 25;237(1):176-85. A cause-effect relationship between these two parameters was established by showing that: (a) rotenone, an inhibitor of complex I, abolished respiration and prevented the enhancement of the DNA-damaging response under all the above circumstances; (b) the membrane-impermeant, complex I-activating substrate gave similar results in permeabilized cells; and (c) none of the -linked substrates affected the DNA-damaging response to tert-butylhydroperoxide in respiration-deficient cells. A cause-effect relationship between these two parameters was established by showing that: (a) rotenone, an inhibitor of complex I, abolished respiration and prevented the enhancement of the DNA-damaging response under all the above circumstances; (b) the membrane-impermeant, complex I-activating substrate gave similar results in permeabilized cells; and (c) none of the -linked substrates affected the DNA-damaging response to tert-butylhydroperoxide in respiration-deficient cells. |
consumption promotes mitochondrial accumulation, a process associated with, and causally 1(0,0,0,1) | Details |
14561532 | Tada-Oikawa S, Hiraku Y, Kawanishi M, Kawanishi S: Mechanism for generation of peroxide and change of mitochondrial membrane potential during rotenone-induced apoptosis. Mitochondrion. 2004 Sep;4(5-6):387-94. Epub 2004 Nov 2. Rotenone, an inhibitor of NADH dehydrogenase complex, is a naturally occurring insecticide, which is capable of inducing apoptosis. |
1(0,0,0,1) | Details |
15342361 | Beretta S, Mattavelli L, Sala G, Tremolizzo L, Schapira AH, Martinuzzi A, Carelli V, Ferrarese C: Leber hereditary optic neuropathy mtDNA mutations disrupt transport in cybrid cell lines. Pediatr Res. 1989 Feb;25(2):194-201. Three pathogenic mutations (positions 11778/ND4, 3460/ND1 and 14484/ND6) account for the majority of LHON cases and they affect genes that encode for different subunits of mitochondrial complex I. |
1(0,0,0,1) | Details |
18036194 | Milusheva E, Baranyi M, Kittel A, Fekete A, Zelles T, Vizi ES, Sperlagh B: Modulation of dopaminergic neurotransmission in rat striatum upon in vitro and in vivo diclofenac treatment. Mol Cells. 2007 Jun 30;23(3):363-9. In conclusion, whereas in vitro DCF pre-treatment resembles the effect of the mitochondrial toxin rotenone, in vivo it rather counteracts than aggravates dopaminergic dysfunction. As it is known that selective mitochondrial complex I inhibition combined with mild oxidative stress causes striatal dopaminergic dysfunction, we tested whether DCF also compromise dopaminergic function in the striatum. [3H] ([3H] DA) release was measured from rat striatal slices after in vitro (2 h, 10-25 micromol/L) or in vivo (3 mg/kg i.v. for 28 days) DCF treatment. |
1(0,0,0,1) | Details |
12950736 | Dell'Anna ML, Urbanelli S, Mastrofrancesco A, Camera E, Iacovelli P, Leone G, Manini P, D'Ischia M, Picardo M: Alterations of mitochondria in peripheral blood mononuclear cells of vitiligo patients. Free Radic Biol Med. 2004 Jan 1;36(1):16-26. Moreover, a marked increase in the expression of mitochondrial malate dehydrogenase activity and a specific sensitivity to electron transport chain complex I inhibitor were observed. |
1(0,0,0,1) | Details |
11961005 | Morigi M, Macconi D, Zoja C, Donadelli R, Buelli S, Zanchi C, Ghilardi M, Remuzzi G: Protein overload-induced NF-kappaB activation in proximal tubular cells requires H (2) O (2) through a PKC-dependent pathway. J Toxicol Environ Health A. 2008;71(24):1582-92. To identify the enzymatic sources responsible for the increased H (2) O (2) production, the effect of dyphenyleneiodonium, an inhibitor of the membrane (H) oxidase, was studied, as was the effect of rotenone, which blocks complex I of the mitochondrial respiratory chain. |
81(1,1,1,1) | Details |
16972982 | Liu L, Li Y, Li H, Chen J: Significant increase of glycolytic flux in Torulopsis glabrata by inhibition of oxidative phosphorylation. Am J Physiol Heart Circ Physiol. 2009 Jan;296(1):H226-32. Epub 2008 Nov 21. One was separately adding, at 10 mg L1, specific inhibitors of complex I (rotenone) or of the bc1 complex (antimycin A) to the culture broth of T. glabrata CCTCC M202019, which resulted in significantly decreased intracellular ATP levels (43% and 27.7%) and significantly increased rates of consumption (qs) and production (qp); another approach was breeding a respiratory-deficient mutant RD-16, in which cytochromes aa3 and b in the ETC were deleted after ethidium mutagenesis, to reduce the ETC activity constitutively. |
81(1,1,1,1) | Details |
19504041 | Pienaar IS, Schallert T, Hattingh S, Daniels WM: Behavioral and quantitative mitochondrial proteome analyses of the effects of neural degeneration. J Neurochem. 2007 Feb;100(3):650-63. Rats were pre-treated with for 14 days, followed by a single unihemispheric (substantia nigra; SN) injection of rotenone, a mitochondrial complex I inhibitor. |
implications for models of 81(1,1,1,1) | Details |
15114628 | Shavali S, Carlson EC, Swinscoe JC, Ebadi M: Parkinsonism-inducing endogenous toxin, increases alpha-synuclein expression and causes nuclear damage in human dopaminergic cells. Int J Biochem Cell Biol. 2008;40(9):1792-805. Epub 2008 Jan 19. Inhibition of complex I by rotenone and depletion of by L-buthionine sulfoxamine also correlated with an increase in alpha-syn expression, suggesting that oxidative stress may cause an increase in alpha-syn levels in dopaminergic cells. |
a 81(1,1,1,1) | Details |
14645467 | Sherer TB, Betarbet R, Testa CM, Seo BB, Richardson JR, Kim JH, Miller GW, Yagi T, Matsuno-Yagi A, Greenamyre JT: Mechanism of toxicity in rotenone models of Parkinson's disease. J Cell Sci. 2007 Dec 1;120(Pt 23):4155-66. Exposure of rats to the pesticide and complex I inhibitor rotenone reproduces features of Parkinson's disease, including selective nigrostriatal dopaminergic degeneration and alpha-synuclein-positive cytoplasmic inclusions (Betarbet et al., 2000; Sherer et al., 2003). |
37(0,1,2,2) | Details |
10354494 | Seo BB, Matsuno-Yagi A, Yagi T: Modulation of oxidative phosphorylation of human kidney 293 cells by transfection with the internal rotenone-insensitive -quinone oxidoreductase (NDI1) gene of Saccharomyces cerevisiae. Biochim Biophys Acta. 1991 Oct 18;1060(2):203-9. The NDI1-transfected HEK 293 cells were able to grow in media containing a complex I inhibitor such as rotenone and 1-methyl-4-phenylpyridinium ion. |
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15469939 | Kweon GR, Marks JD, Krencik R, Leung EH, Schumacker PT, Hyland K, Kang UJ: Distinct mechanisms of neurodegeneration induced by chronic complex I inhibition in dopaminergic and non-dopaminergic cells. J Neurochem. 2002 Oct;83(1):220-8. To elucidate the mechanisms of chronic complex I disruption-induced neurodegeneration, we induced differentiation of immortalized midbrain dopaminergic (MN9D) and non-dopaminergic (MN9X) neuronal cells, to maintain them in culture without significant cell proliferation and compared their survivals following chronic exposure to nanomolar rotenone, an irreversible complex I inhibitor. |
34(0,1,1,4) | Details |
3094534 | Suzuki H, Wakai M, Ozawa T: Selective inhibition of mitochondrial -ubiquinone reductase (Complex I) by an alkyl polyoxyethylene ether. J Appl Physiol. 2008 Oct;105(4):1114-26. Epub 2008 Aug 14. Partial removal of phospholipids from Complex I from 18.8% (w/w) to 14.5% significantly decreased its susceptibility to the inhibitor as well as to rotenone. |
34(0,1,1,4) | Details |
8806050 | Sablin SO, Krueger MJ, Yankovskaya VL, Tkachenko SE, Razdolsky AN, Bachurin SO, Ramsay RR, Singer TP: Inhibition of oxidation by 1-methyl-4-phenylpyridinium analogs as the basis for the prediction of the inhibitory potency of novel compounds. J Biochem Toxicol. 1996;11(1):33-43. The IC50 values for these compounds and previously published figures for MPP+ analogs were then used to select a computer model based on structural parameters to predict the inhibitory potency of other compounds that react at the "rotenone site" in Complex I. |
32(0,1,1,2) | Details |
17854275 | Doughan AK, Dikalov SI: Mitochondrial redox cycling of mitoquinone leads to production and cellular apoptosis. Biochim Biophys Acta. 1997 Jul 4;1320(3):256-64. Inhibitor analysis suggested that the redox cycling of MitoQ occurred at two sites on complex I, proximal and distal to the rotenone-binding site. |
32(0,1,1,2) | Details |
20064719 | Geldenhuys WJ, Funk MO, Barnes KF, Carroll RT: Structure-based design of a thiazolidinedione which targets the mitochondrial protein mitoNEET. Bioorg Med Chem Lett. 2010 Feb 1;20(3):819-23. Epub 2010 Jan 4. To investigate the ability of NL-1 to block rotenone initiated free radicals from complex I, we found it was able to protect the human neuronal cell line SH-SY5Y against rotenone induced cell death. |
32(0,1,1,2) | Details |
19339632 | Huang S, Zhang A, Ding G, Chen R: mediated by EGF receptor transactivation. Am J Physiol Renal Physiol. 2009 Jun;296(6):F1323-33. Epub 2009 Apr 1. Pretreatment with the antioxidant N-acetyl- catalase, SOD, mitochondrial respiratory chain complex I inhibitor rotenone (Rot), oxidase inhibitor apocynin, and DPI significantly inhibited Aldo-stimulated MC proliferation as well as EGFR transactivation. |
-induced mesangial cell proliferation is 31(0,1,1,1) | Details |
16668549 | Luethy MH, Hayes MK, Elthon TE: Partial Purification and Characterization of Three NAD (P) H Dehydrogenases from Beta vulgaris Mitochondria. Plant Physiol. 1991 Dec;97(4):1317-1322. All three peaks are insensitive to divalent cation chelators and a complex I inhibitor, rotenone. |
31(0,1,1,1) | Details |
9586799 | Tsai MJ, Lee EH: astrocytes from 1-methyl-4-phenylpyridinium-induced toxicity. Free Radic Biol Med. 1998 Mar 15;24(5):705-13. NO. donors and analogues were also tested against damage produced by rotenone, an irreversible complex I inhibitor. |
donors protect cultured rat 31(0,1,1,1) | Details |
17207576 | Thompson RJ, Buttigieg J, Zhang M, Nurse CA: A rotenone-sensitive site and H2O2 are key components of hypoxia-sensing in neonatal rat adrenomedullary chromaffin cells. J Neurol Sci. 2005 May 15;232(1-2):95-103. Of several mitochondrial electron transport chain (ETC) inhibitors tested, only rotenone, a complex I blocker, mimicked and occluded the effects of hypoxia on outward current, cellular ROS, and ATP secretion. |
31(0,1,1,1) | Details |
17673201 | Tozzi A, Costa C, Di Filippo M, Tantucci M, Siliquini S, Belcastro V, Parnetti L, Picconi B, Calabresi P: Memantine reduces neuronal dysfunctions triggered by in vitro ischemia and 3-nitropropionic acid. Biochim Biophys Acta. 2010 Feb 17. Moreover, memantine showed protection against irreversible field potential loss induced by 3-nitropropionic acid (3-NP), an inhibitor of the mitochondrial complex II, without influencing toxicity induced by rotenone, a complex I inhibitor. |
31(0,1,1,1) | Details |
15794752 | Falchi AM, Isola R, Diana A, Putzolu M, Diaz G: Characterization of depolarization and repolarization phases of mitochondrial membrane potential fluctuations induced by tetramethylrhodamine methyl ester photoactivation. Biochem J. 2003 May 1;371(Pt 3):1005-11. The frequency of R phases was significantly inhibited by oligomycin and aurovertin (mitochondrial ATP synthase inhibitors), rotenone (mitochondrial complex I inhibitor) and iodoacetic acid (inhibitor of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase). |
31(0,1,1,1) | Details |
8078526 | Beattie DS, Obungu VH, Kiaira JK: Oxidation of by a rotenone and antimycin-sensitive pathway in the mitochondrion of procyclic Trypanosoma brucei brucei. Biochem Biophys Res Commun. 1994 Nov 30;205(1):264-8. Both NADH:cytochrome c and NADH:ubiquinone reductase activities were inhibited 80-90% by rotenone indicating the presence of a complex I-like NADH dehydrogenase in the mitochondrion of trypanosomes. |
31(0,1,1,1) | Details |
11909981 | Schapira AH: Neuroprotection and agonists. . J Physiol. 2003 May 1;548(Pt 3):789-800. Epub 2003 Mar 7. Neuronal toxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can induce parkinsonism in human and animal models, and rotenone, another specific mitochondrial complex I inhibitor, can induce similar effects in rodents to produce a model for PD. |
31(0,1,1,1) | Details |
15992782 | Sindhu KM, Saravanan KS, Mohanakumar KP: Behavioral differences in a rotenone-induced hemiparkinsonian rat model developed following intranigral or median forebrain bundle infusion. J Biol Chem. 1997 Apr 11;272(15):9605-8. A mitochondrial complex-I inhibitor, rotenone was unilaterally infused into the substantia nigra pars compacta (SNpc) or median forebrain bundle (MFB) to create hemiparkinsonian animal models and investigated spontaneous and drug-induced stereotypic rotations, as well as certain postural behaviors in Sprague-Dawley rats. |
31(0,1,1,1) | Details |
11728422 | Yuki K, Suzuki T, Katoh S, Kakinuma Y, Miyauchi T, Mitsui Y: Endothelin-1 stimulates cardiomyocyte injury during mitochondrial dysfunction in culture. Int J Biochem Cell Biol. 2008;40(10):2098-109. Epub 2008 Feb 16. Primary cultured cardiomyocytes from neonatal rats were pretreated with rotenone, a mitochondrial complex I inhibitor, and the cytotoxic effect of endothelin-1 on the cardiomyocytes was demonstrated. |
31(0,1,1,1) | Details |
3110216 | Hoppel CL, Kerr DS, Dahms B, Roessmann U: Deficiency of the complex I of mitochondrial electron transport. Biol Bull. 2007 Apr;212(2):169-75. Mitochondrial NADH dehydrogenase activity (complex I, assayed as rotenone-sensitive oxidase, -duroquinone reductase, and -cytochrome c reductase) was 0-10% of controls, and -ferricyanide reductase activity was 25-50% of controls in the mitochondria and in skin fibroblasts. |
dehydrogenase component of 13(0,0,2,3) | Details |
8192914 | Birch-Machin MA, Briggs HL, Saborido AA, Bindoff LA, Turnbull DM: An evaluation of the measurement of the activities of complexes I-IV in the respiratory chain of human skeletal muscle mitochondria. Int Immunol. 1997 Jun;9(6):835-41. Complex I activity is measured in the presence of 2.5 mg.ml-1 bovine serum albumin, which increases rotenone sensitivity, and we have shown that NADH-cytochrome b5 reductase makes an important contribution to the rotenone-insensitive NADH-ubiquinone oxidoreductase activity. |
7(0,0,1,2) | Details |
6460022 | Schwitzguebel JP, Palmer JM: Properties of mitochondria as a function of the growth stages of Neurospora crassa. Anal Biochem. 1995 Sep 1;230(1):16-9. One pathway was sensitive to rotenone and involved three energy-coupling sites, whereas the other was resistant to rotenone and bypassed complex I. |
7(0,0,1,2) | Details |
14670598 | Grivennikova VG, Roth R, Zakharova NV, Hagerhall C, Vinogradov AD: The mitochondrial and prokaryotic NADH:ubiquinone oxidoreductases: similarities and dissimilarities of the -junction sites. J Bacteriol. 1982 Feb;149(2):612-9. The catalytic properties of the rotenone-sensitive NADH:ubiquinone reductase (Complex I) in bovine heart submitochondrial particles and in inside-out vesicles derived from Paracoccus denitrificans and Rhodobacter capsulatus were compared. |
-translocating 7(0,0,1,2) | Details |
11080215 | Talpade DJ, Greene JG, Higgins DS Jr, Greenamyre JT: In vivo labeling of mitochondrial complex I (NADH:ubiquinone oxidoreductase) in rat brain using [(3) H] dihydrorotenone. Biochem Pharmacol. 2001 Mar 1;61(5):547-54. In vivo [(3) H] DHR binding was markedly reduced by local and systemic infusion of rotenone and was enhanced by local administration. |
4(0,0,0,4) | Details |
11325348 | Cormier A, Morin C, Zini R, Tillement JP, Lagrue G: In vitro effects of bound to complex I of the respiratory chain and inhibited the -Ubiquinone reductase activity. |
on mitochondrial respiration and generation. 131-40.4(0,0,0,4) | Details |
18817789 | Abdin AA, Hamouda HE: Mechanism of the neuroprotective role of with or without in rotenone-induced parkinsonism. IUBMB Life. 2001 Sep-Nov;52(3-5):135-41. This model confirmed the implication of mitochondrial-apoptotic pathway in the pathogenesis of parkinsonism as there was a decrease in levels of striatal complex I activity and ATP as well as extreme overexpression of the antiapoptotic protein Bcl-2, and also exhibited the role of where its plasma and striatal levels were found to be decreased in comparison to the normal control rats (group I). |
3(0,0,0,3) | Details |
12914921 | Grivennikova VG, Ushakova AV, Cecchini G, Vinogradov AD: Unidirectional effect of lauryl NADH:ubiquinone oxidoreductase (Complex I). Biochem Biophys Res Commun. 1992 Nov 30;189(1):47-52. The inhibitor affects neither oxidase (coupled or uncoupled) nor NADH:ferricyanide reductase and oxidase activities at the concentrations that selectively prevent the -supported, rotenone-sensitive (+) or ferricyanide reduction. |
on the reversible 3(0,0,0,3) | Details |
8312726 | Yamada K, Fukushima T: Mechanism of cytotoxicity of paraquat. J Clin Endocrinol Metab. 2008 Aug;93(8):3199-207. Epub 2008 May 20. Paraquat also stimulated O2- production in bovine liver NADH-ubiquinone oxidoreductase (complex I). O2- production was stimulated by paraquat even in the presence of rotenone, one of the mitochondrial respiratory chain inhibitors. |
2(0,0,0,2) | Details |
12607133 | Bernocchi P, Cargnoni A, Vescovo G, Dalla Libera L, Parrinello G, Boraso A, Ceconi C, Ferrari R: Skeletal muscle abnormalities in rats with experimentally induced heart hypertrophy and failure. Toxicol Appl Pharmacol. 2007 Jun 1;221(2):222-34. Epub 2007 Mar 23. Activity of the different complexes of respiratory chain was investigated by means of specific inhibitors, showing major abnormalities at the level of complex I. In fact, inhibition of VO (2) by rotenone was decreased from 83.5 +/- 3.2 to 36.4 +/- 9.6 % (p < 0.005) and from 81.8 +/- 6.1 to 38.2 +/- 7.4 % (p < 0.005) in soleus and EDL, respectively. |
2(0,0,0,2) | Details |
10650131 | Storch A, Kaftan A, Burkhardt K, Schwarz J: neuroblastoma SH-SY5Y cells via impairment of cellular energy metabolism. Chem Biol Interact. 1997 Aug 29;106(1):15-28. The endogenous neurotoxin 1-methyl-6,7-dihydroxy-1,2,3, 4-tetrahydroisoquinoline which is structurally similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has been reported to inhibit mitochondrial complex I -Q reductase) activity as does the MPTP metabolite 1-methyl-4-phenylpyridinium ion (MPP (+)). |
is toxic to dopaminergic 1(0,0,0,1) | Details |
11812926 | Mildaziene V, Nauciene Z, Baniene R, Grigiene J: Multiple effects of 2,2',5,5'-tetrachlorobiphenyl on oxidative phosphorylation in rat liver mitochondria. J Biol Chem. 2004 Sep 17;279(38):39414-20. Epub 2004 Jul 15. An experimental investigation of the response of the multicomponent oxidative phosphorylation system to the environmental pollutant 2,2',5,5'-tetrachlorobiphenyl (2,2',5,5'-TCB) was performed by modular kinetic analysis in rat liver mitochondria oxidizing (+ rotenone) and + We explain this by the 2,2',5,5'-TCB-induced inhibition of Complex I. |
1(0,0,0,1) | Details |
16584562 | Zhao Z, Lange DJ, Voustianiouk A, MacGrogan D, Ho L, Suh J, Humala N, Thiyagarajan M, Wang J, Pasinetti GM: A ketogenic diet as a potential novel therapeutic intervention in amyotrophic lateral sclerosis. BMC Neurosci. 2006 Apr 3;7:29. DBH prevented rotenone mediated inhibition of mitochondrial complex I but not inhibition of complex II. These effects may be due to the ability of ketone bodies to promote ATP synthesis and bypass inhibition of complex I in the mitochondrial respiratory chain. |
1(0,0,0,1) | Details |
1313376 | Ahmed I, Krishnamoorthy G: The non-equivalence of binding sites of coenzyme and rotenone in mitochondrial - reductase. Cell Physiol Biochem. 2008;22(5-6):475-86. Epub 2008 Dec 9. The fluorescent probe erythrosine 5'-iodoacetamide (ER) binds to mitochondrial - reductase (Complex-I) accompanied by an enhancement of the fluorescence intensity. |
1(0,0,0,1) | Details |
15265640 | Alam M, Schmidt WJ: rotenone-treated rats. Biochem Med Metab Biol. 1994 Feb;51(1):35-42. Peripherally and locally administered rotenone (an inhibitor of mitochondrial complex I) has been proposed as a model of Parkinson's disease (PD) as it induces nigrostriatal degeneration associated with alpha-synuclein inclusions. |
reverses the hypokinetic behaviour and rigidity in 1(0,0,0,1) | Details |
14653820 | Jasso-Chavez R, Moreno-Sanchez R: Cytosol-mitochondria transfer of reducing equivalents by a lactate shuttle in heterotrophic Euglena. Biochem Soc Symp. 1999;66:85-97. an inhibitor of iLDH, strongly inhibited oligomycin-sensitive respiration and growth, whereas rotenone, an inhibitor of respiratory complex I, only slightly affected these parameters in lactate-grown cells. an inhibitor of iLDH, strongly inhibited oligomycin-sensitive respiration and growth, whereas rotenone, an inhibitor of respiratory complex I, only slightly affected these parameters in lactate-grown cells. |
1(0,0,0,1) | Details |
9221826 | Corsini E, Viviani B, Marinovich M, Galli CL: Role of mitochondria and ions in tributyltin-induced gene regulatory pathways. Neurobiol Dis. 2006 Nov;24(2):308-17. Epub 2006 Sep 7. Furthermore, the modulation of cellular oxidative activity induced by TBT observed with rotenone, an inhibitor of the electron entry from complex I to or after prolonged treatment with ethidium an inhibitor of mitochondrial DNA and RNA synthesis, indicates mitochondria as an important intracellular source of reactive species. Furthermore, the modulation of cellular oxidative activity induced by TBT observed with rotenone, an inhibitor of the electron entry from complex I to or after prolonged treatment with ethidium an inhibitor of mitochondrial DNA and RNA synthesis, indicates mitochondria as an important intracellular source of reactive species. |
1(0,0,0,1) | Details |
12220540 | Belyaeva EA, Glazunov VV, Korotkov SM: Cyclosporin A-sensitive permeability transition pore is involved in Cd (2+)-induced dysfunction of isolated rat liver mitochondria: doubts no more. J Neural Transm. 2010 Jan;117(1):5-12. Epub 2009 Aug 26. There is dose-dependent Cd (2+)-evoked swelling of isolated rat liver mitochondria energized by complex I, II, or IV respiratory substrates in medium in the absence of added Ca (2+) and P (i), which is prevented by Sr (2+). Sustained activation by low [Cd (2+)] of mitochondrial basal respiration in KCl medium is observed both in the absence and in the presence of rotenone and/or oligomycin but only in the latter case (rotenone+oligomycin) CsA inhibits completely Cd (2+) activation of St 4 respiration and partially reverses DNP-uncoupled respiration depressed by cadmium. |
1(0,0,0,1) | Details |
7622334 | Armson A, Grubb WB, Mendis AH: The effect of electron transport (ET) inhibitors and thiabendazole on the reductase (FR) and succinate dehydrogenase (SDH) of Strongyloides ratti infective (L3) larvae. Neurotoxicology. 2009 Nov;30(6):977-85. Epub 2009 Sep 8. Rotenone (a specific inhibitor of electron transport Complex I) inhibited the S. ratti FR (EC50 = 3.0 x 10 (-7) M) but not SDH. This strongly suggests that the S. ratti FR is functionally linked with the S. ratti ET-Complex I. 2-Thenoyltrifluoroacetone (TTFA, an inhibitor of ET-Complex II) inhibited FR (EC50 = 2.6 x 10 (-5) M) and SDH (EC50 = 2.8 x 10 (-5) M) with similar effectiveness. |
1(0,0,0,1) | Details |
17023676 | Saitoh S, Zhang C, Tune JD, Potter B, Kiyooka T, Rogers PA, Knudson JD, Dick GM, Swafford A, Chilian WM: couples myocardial metabolism to coronary blood flow. J Neurochem. 2007 Mar;100(6):1469-79. Epub 2007 Jan 4. METHODS AND RESULTS: The production of O2*- is coupled to oxidative metabolism because inhibition of complex I (rotenone) or III (antimycin) enhanced the production of O2*- during pacing by about 50% and 400%, respectively; whereas uncoupling oxidative phosphorylation by decreasing the protonmotive force with carbonylcyanide-p-trifluoromethoxyphenyl-hydrazone (FCCP) decreased pacing-induced O2*- production. |
peroxide: a feed-forward dilator that 81(1,1,1,1) | Details |
17429617 | Xiong K, Cai H, Luo XG, Struble RG, Clough RW, Yan XX: Mitochondrial respiratory inhibition and oxidative stress elevate beta-secretase (BACE1) proteins and activity in vivo in the rat retina. Am J Physiol Heart Circ Physiol. 2008 Jul;295(1):H281-8. Epub 2008 May 16. Retinas were analyzed biochemically and anatomically 48 h following intraocular applications of mitochondrial complex I, II and IV inhibitors including rotenone, 3-nitropropionic acid and azide, and plaque-containing oxidants including Fe (3+) and Abeta42 fibrils (Abeta42f). |
81(1,1,1,1) | Details |
17477947 | Hansen T, Seidel A, Borlak J: The environmental carcinogen 3-nitrobenzanthrone and its main metabolite 3-aminobenzanthrone enhance formation of reactive intermediates in human A549 lung epithelial cells. J Neurol Sci. 1999 May 1;165(1):10-7. Mitochondrial ROS production was significantly attenuated (20% reduction) by addition of rotenone (complex I inhibition) and thenoyltrifluoroacetone (TTFA, complex II inhibition). |
81(1,1,1,1) | Details |
11826108 | Gao HM, Hong JS, Zhang W, Liu B: Distinct role for microglia in rotenone-induced degeneration of dopaminergic neurons. Biochim Biophys Acta. 2006 May-Jun;1757(5-6):708-14. Epub 2006 Feb 24. In experimental animals the exposure to a common herbicide, rotenone, induces features of parkinsonism; mechanistically, rotenone-induced destruction of dopaminergic neurons has been attributed to its inhibition of the activity of neuronal mitochondrial complex I. |
81(1,1,1,1) | Details |
14976342 | Newhouse K, Hsuan SL, Chang SH, Cai B, Wang Y, Xia Z: Rotenone-induced apoptosis is mediated by p38 and JNK MAP kinases in human dopaminergic SH-SY5Y cells. Biochim Biophys Acta. 2008 Nov;1777(11):1455-62. Epub 2008 Aug 22. Though rotenone is known to be an inhibitor of the mitochondrial complex I electron transport chain, little is known about downstream pathways leading to its toxicity. |
81(1,1,1,1) | Details |
12018892 | Nakashima Y, Shinzawa-Itoh K, Watanabe K, Naoki K, Hano N, Yoshikawa S: The second binding site of bovine heart oxidoreductase. Int J Parasitol. 1995 Feb;25(2):261-3. The rotenone-insensitive Complex I reaction in Q1 concentration range above 300 microM indicates an ordered sequential mechanism with Q1 and reduced Q1 (Q1H2) as the initial substrate to bind to the enzyme and the last product to be released from the enzyme product complex, respectively. |
37(0,1,2,2) | Details |
16490285 | Saravanan KS, Sindhu KM, Senthilkumar KS, Mohanakumar KP: L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats. Plant Physiol. 1984 Jun;75(2):414-420. The present study investigated oxidative damage and neuroprotective effect of the antiparkinsonian drug, L-deprenyl in neuronal death produced by intranigral infusion of a potent mitochondrial complex-I inhibitor, rotenone in rats. |
37(0,1,2,2) | Details |
14625276 | Kudin AP, Bimpong-Buta NY, Vielhaber S, Elger CE, Kunz WS: Characterization of brain mitochondria. J Physiol. 2004 May 1;556(Pt 3):755-71. Epub 2004 Feb 6. Although rat brain mitochondria in the presence of glutamate+malate alone do generate only small amounts of H2O2 (0.04 +/- 0.02 nmol H2O2/min/mg), a substantial production is observed after the addition of the complex I inhibitor rotenone (0.68 +/- 0.25 nmol H2O2/min/mg) or in the presence of the respiratory substrate alone (0.80 +/- 0.27 nmol H2O2/min/mg). |
-producing sites in isolated 34(0,1,1,4) | Details |
16959493 | Beretta S, Wood JP, Derham B, Sala G, Tremolizzo L, Ferrarese C, Osborne NN: Partial mitochondrial complex I inhibition induces oxidative damage and perturbs transport in primary retinal cultures. Brain Res Brain Res Protoc. 2001 Jul;7(3):267-76. Primary rat retinal cultures were exposed to increasing concentrations of rotenone to titrate complex I inhibition. |
34(0,1,1,4) | Details |
15953813 | Naoi M, Maruyama W, Shamoto-Nagai M, Yi H, Akao Y, Tanaka M: Oxidative stress in mitochondria: decision to survival and death of neurons in neurodegenerative disorders. Proteomics. 2007 Jun;7(13):2189-200. The interactions among these factors were studied by use of a -generating agent, N-morpholino sydnonimine (SIN-1) and an inhibitor of complex I, rotenone, in human dopaminergic SH-SY5Y cells. |
32(0,1,1,2) | Details |
7586047 | Landolt JL, Ahammadsahib KI, Hollingworth RM, Barr R, Crane FL, Buerck NL, McCabe GP, McLaughlin JL: Determination of structure-activity relationships of Annonaceous acetogenins by inhibition of uptake in rat liver mitochondria. Biochemistry. 2001 Apr;66(4):435-43. A new group of natural compounds, the Annonaceous acetogenins, have recently been determined to inhibit ATP production at a similar site of action and higher levels of potency as rotenone, i.e., at - oxido-reductase, complex I of the mitochondrial electron-transport chain. |
32(0,1,1,2) | Details |
18848925 | Ying R, Liang HL, Whelan HT, Eells JT, Wong-Riley MT: Pretreatment with near-infrared light via light-emitting diode provides added benefit against rotenone- and MPP+-induced neurotoxicity. Am J Physiol. 1996 Nov;271(5 Pt 2):H1893-9. The present study used these specific mitochondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP (+)) on striatal and cortical neurons in culture. |
32(0,1,1,2) | Details |
15893762 | Shneyvays V, Leshem D, Shmist Y, Zinman T, Shainberg A: Effects of derivative on cultured cardiomyocytes with mitochondrial disorders. Plant Physiol. 1988 Apr;86(4):1199-1204. As was shown in this study, 3 microM of AK-135 restored ATP production after blockade of electron flow through mitochondrial complex I with 5 microM rotenone up to 13.18+/-1.56 vs. 3.21+/-1.12 nmol/mg protein in cells treated with rotenone only. |
and its 31(0,1,1,1) | Details |
1847635 | Demant EJ: Inactivation of cytochrome c oxidase activity in mitochondrial membranes during redox cycling of doxorubicin. FEBS Lett. 2004 Jan 2;556(1-3):111-5. It is related in a complex manner to the electron flux in the respiratory chain with antioxidant properties, and is maximal at the high reduction level of respiratory chain Complex I obtained in the presence of rotenone. |
31(0,1,1,1) | Details |
2871147 | Sugiyama Y, Fujita T, Matsumoto M, Okamoto K, Imada I: Effects of idebenone (CV-2619) and its metabolites on respiratory activity and lipid peroxidation in brain mitochondria from rats and dogs. J Neurosci Res. 2000 May 15;60(4):552-8. These facts and results of inhibitor analysis suggest that the action site of CV-2619 is -linked complex I in the mitochondrial respiratory chain and is different from that of inhibitors of oxidative phosphorylation such as rotenone, oligomycin and 2,4-dinitrophenol. |
31(0,1,1,1) | Details |
10762084 | Chinopoulos C, Tretter L, Adam-Vizi V: Reversible depolarization of in situ mitochondria by oxidative stress parallels a decrease in NAD (P) H level in nerve terminals. J Pharmacobiodyn. 1985 Dec;8(12):1006-17. The effect of H2O2 on delta (psi) m in the presence of the complex I inhibitor, rotenone, was also unaltered by addition of catalase. |
31(0,1,1,1) | Details |
18804145 | Kaneko K, Hineno A, Yoshida K, Ikeda S: Increased vulnerability to rotenone-induced neurotoxicity in ceruloplasmin-deficient mice. J Biochem. 1983 Oct;94(4):1301-6. Rotenone, a selective mitochondrial complex I inhibitor, induces neurodegeneration mimicking Parkinson's disease. |
31(0,1,1,1) | Details |
15729575 | Artwohl M, Furnsinn C, Waldhausl W, Holzenbein T, Rainer G, Freudenthaler A, Roden M, Baumgartner-Parzer SM: Thiazolidinediones inhibit proliferation of microvascular and macrovascular cells by a PPARgamma-independent mechanism. Curr Alzheimer Res. 2009 Sep 28. Proliferation inhibition and lactate release were mimicked by rotenone (mitochondrial complex I inhibitor). |
31(0,1,1,1) | Details |
19445904 | Huang J, Hao L, Xiong N, Cao X, Liang Z, Sun S, Wang T: Involvement of glyceraldehyde-3-phosphate dehydrogenase in rotenone-induced cell apoptosis: relevance to protein misfolding and aggregation. J Neurochem. 2004 Jul;90(2):405-21. We found that rotenone, a common mitochondrial complex I inhibitor used to produce experimental parkinsonism, cannot only induce GAPDH translocation but also trigger intermolecular disulfide bonding and result in the formation of intracytoplasmic aggregates of GAPDH. |
31(0,1,1,1) | Details |
12919951 | Liu Y, Zhao H, Li H, Kalyanaraman B, Nicolosi AC, Gutterman DD: Mitochondrial sources of H2O2 generation play a key role in flow-mediated dilation in human coronary resistance arteries. Invest Ophthalmol Vis Sci. 2008 Apr;49(4):1447-58. Diameter changes to increases in pressure gradients (20 and 100 cm were examined in the absence and the presence of rotenone (1 micromol/L), myxothiazol (100 nmol/L), (1 micromol/L), mitochondrial complex I, III, and IV inhibitors, respectively, and apocynin (3 mmol/L), a oxidase inhibitor. |
31(0,1,1,1) | Details |
9614211 | De Kimpe SJ, Anggard EE, Carrier MJ: Reactive macrophage scavenger receptor type I, but not type II, in the human monocytic cell line THP-1. PLoS One. 2010 Mar 10;5(3):e9532. Several sources of reactive species are involved as inhibition of MSR activity and levels of MSR-I mRNA occurred in the presence of rotenone, a mitochondrial complex I inhibitor, or acetovanillone, a oxidase inhibitor. |
species regulate 31(0,1,1,1) | Details |
16686429 | Lopez-Barneo J, Ortega-Saenz P, Piruat JI, Garcia-Fernandez M: function in carotid body glomus cells. J Neurochem. 2005 Nov;95(4):930-9. Epub 2005 Aug 10. However, rotenone, a complex I blocker, selectively occludes the responsiveness to hypoxia of glomus cells in a dose-dependent manner. |
-sensing by ion channels and mitochondrial 6(0,0,1,1) | Details |
19220002 | King MS, Sharpley MS, Hirst J: Reduction of hydrophilic ubiquinones by the flavin in mitochondrial NADH:ubiquinone oxidoreductase (Complex I) and production of reactive species. J Neurosci Res. 2003 Nov 15;74(4):589-97. Hydrophilic ubiquinones are reduced by an additional, non-energy-transducing pathway (which is insensitive to inhibitors such as rotenone and piericidin A). |
6(0,0,0,6) | Details |
12351220 | Helmerhorst EJ, Murphy MP, Troxler RF, Oppenheim FG: Characterization of the mitochondrial respiratory pathways in Candida albicans. Eur J Biochem. 1996 Nov 1;241(3):888-94. In addition, / respiration was rotenone-sensitive, and an enzyme activity assay further confirmed that C. albicans cells express Complex I activity. |
6(0,0,1,1) | Details |
3134026 | Tanaka M, Nishikimi M, Suzuki H, Ozawa T, Ichiki T, Kobayashi M, Wada Y: Variation in the levels of complex I subunits among tissues in a patient with mitochondrial encephalomyopathy and renal dysfunction. Am J Physiol Lung Cell Mol Physiol. 2002 Nov;283(5):L922-31. Rotenone-sensitive -cytochrome c reductase activity was decreased in all the tissues examined, but the degree of deficiency varied from tissue to tissue. |
4(0,0,0,4) | Details |
20074573 | Nakamaru-Ogiso E, Han H, Matsuno-Yagi A, Keinan E, Sinha SC, Yagi T, Ohnishi T: The ND2 subunit is labeled by a photoaffinity analogue of asimicin, a potent complex I inhibitor. Neurochem Res. 2009 Aug;34(8):1469-78. Epub 2009 Feb 28. The cross-linking was blocked by rotenone. |
4(0,0,0,4) | Details |
8443212 | Sled VD, Vinogradov AD: Kinetics of the mitochondrial NADH-ubiquinone oxidoreductase interaction with hexammineruthenium (III). Trends Neurosci. 2001 May;24(5):245-7. Qualitatively the same results were obtained using submitochondrial particles or isolated Complex I. Both hexammineruthenium (III) and ferricyanide reduction was rotenone-insensitive and showed no stimulation by the uncouplers in tightly coupled submitochondrial particles. |
3(0,0,0,3) | Details |
7957254 | Finel M, Majander AS, Tyynela J, De Jong AM, Albracht SP, Wikstrom M: Isolation and characterisation of subcomplexes of the mitochondrial NADH:ubiquinone oxidoreductase (complex I). Nat Neurosci. 2000 Dec;3(12):1301-6. In addition, the Q-1 reductase activity of all the subcomplexes is insensitive to rotenone. |
3(0,0,0,3) | Details |
3106581 | Nishizawa M, Tanaka K, Shinozawa K, Kuwabara T, Atsumi T, Miyatake T, Ohama E: A mitochondrial encephalomyopathy with cardiomyopathy. Neurology. 2002 Feb 26;58(4 Suppl 1):S9-18. A case revealing a defect of complex I in the respiratory chain.. The rotenone-sensitive NADH-coenzyme Q reductase activity was markedly decreased in heart, skeletal muscle and liver mitochondria. |
3(0,0,0,3) | Details |
14972026 | Johansson FI, Michalecka AM, Moller IM, Rasmusson AG: Oxidation and reduction of nucleotides in alamethicin-permeabilized plant mitochondria. Drugs Exp Clin Res. 1999;25(2-3):87-97. AlaM was found to inhibit the electron-transport chain at the external Ca2+-dependent rotenone-insensitive NADH dehydrogenase and around complexes III and IV. Nevertheless, under optimal conditions, especially complex I-mediated oxidation in AlaM-treated mitochondria was much higher than what has been previously measured by other techniques. |
2(0,0,0,2) | Details |
16917840 | Imamura K, Takeshima T, Kashiwaya Y, Nakaso K, Nakashima K: D-rotenone model of Parkinson's disease. J Neurochem. 1996 Apr;66(4):1617-24. Rotenone, an inhibitor of mitochondrial complex I, provides models of PD both in vivo and in vitro. |
protects dopaminergic SH-SY5Y cells in a 2(0,0,0,2) | Details |
1645458 | Bienen EJ, Saric M, Pollakis G, Grady RW, Clarkson AB Jr: Mitochondrial development in Trypanosoma brucei brucei transitional bloodstream forms. Toxicol Sci. 2002 Feb;65(2):220-7. The EMF is inhibited by 2,4-dinitrophenol, rotenone and salicylhydroxamic acid but not by antimycin A or This putative production is either by F1F0 ATPase driven by the complex I proton pump or by mitochondrial substrate level phosphorylation, or most likely by both. |
1(0,0,0,1) | Details |
11696188 | Svensson AS, Rasmusson AG: Light-dependent gene expression for proteins in the respiratory chain of potato leaves. Biochem J. 2007 Aug 15;406(1):125-9. The recently characterized nda1 and ndb1 genes, homologues to genes encoding the non- pumping respiratory chain NADH-dehydrogenases of Escherichia coli and yeast, were compared to genes encoding catalytic subunits of the -pumping NADH dehydrogenase (complex I). As leaves develop from young to mature, the nda1 transcript level increases, accompanied by an elevation in immunodetected NDA protein and internal rotenone-insensitive oxidation. |
1(0,0,0,1) | Details |
18802751 | Xiong Y, Ding H, Xu M, Gao J: Protective effects of asiatic acid on rotenone- or H2O2-induced injury in SH-SY5Y cells. FEBS Lett. 1992 Apr 6;300(3):275-8. Mitochondrial dysfunction occurred in PD patients showing a 15-30% loss of activity in complex I. |
1(0,0,0,1) | Details |
9070626 | Sriram K, Pai KS, Boyd MR, Ravindranath V: Evidence for generation of oxidative stress in brain by MPTP: in vitro and in vivo studies in mice. J Neurochem. 2002 Dec;83(5):1094-102. In the striatum significant inhibition of rotenone-sensitive oxido-reductase (Complex 1) was observed transiently 1 h after MPTP administration. The enzyme activity recovered thereafter; significant inhibition of mitochondrial Complex I was observed in the striatum only 18 h after MPTP dose. |
1(0,0,0,1) | Details |
11064159 | Lopez-Torres M, Romero M, Barja G: Effect of thyroid hormones on mitochondrial free radical production and DNA oxidative damage in the rat heart. Antioxid Redox Signal. 2005 May-Jun;7(5-6):630-8. Studies with respiratory inhibitors showed that the decrease in radical generation observed in hypothyroidism occurred at Complex III (mainly) and at Complex I; that decrease was due to the presence of a lower free radical leak in the respiratory chain (P <0.05). |
1(0,0,0,1) | Details |
17027047 | Watabe M, Nakaki T: ATP depletion does not account for apoptosis induced by inhibition of mitochondrial electron transport chain in human dopaminergic cells. Ann Neurol. 2008 Nov;64(5):555-65. To date, ETC complex (I-IV) inhibitors (ETCIs) have been thought to induce ATP depletion, triggering cellular apoptosis. In human dopaminergic SH-SY5Y cells, ETCIs (rotenone, thenoyltrifluoroacetone, antimycin A and depleted ATP and induced apoptosis. |
1(0,0,0,1) | Details |
16344601 | French SW: The pathogenesis and significance of the urinary When complex I (NADH dehydrogenase) of the mitochondrial electron transport chain is inhibited by feeding rotenone, the cycle is totally eliminated and blood levels remain constant at 200 mg/%. |
cycle in rats fed intragastrically. Alcohol Clin Exp Res. 2005 Nov;29(11 Suppl):158S-161S.81(1,1,1,1) | Details |
20089711 | Zoer B, Cogolludo AL, Perez-Vizcaino F, De Mey JG, Blanco CE, Villamor E: Hypoxia sensing in the fetal chicken femoral artery is mediated by the mitochondrial electron transport chain. Brain Res. 2000 Feb 7;855(1):67-75. Hypoxia-induced relaxation was abolished or significantly reduced by the mETC inhibitors rotenone (complex I), myxothiazol and antimycin A (complex III), and NaN (3) (complex IV). |
81(1,1,1,1) | Details |
12601064 | Yang JH, Basinger SF, Gross RL, Wu SM: Blue light-induced generation of reactive transport. J Inherit Metab Dis. 1996;19(5):675-86. Rotenone or antimycin A, the respiratory electron transport blockers at complex I and III, respectively, significantly suppressed the light-evoked generation of rOx. |
species in photoreceptor ellipsoids requires mitochondrial electron 81(1,1,1,1) | Details |
19616571 | Alam M, Danysz W, Schmidt WJ, Dekundy A: Effects of receptor antagonists on the development of neurotoxicity produced by chronic rotenone in rats. Biochim Biophys Acta. 2004 Oct 4;1658(3):244-51. Systemic inhibition of complex I by rotenone in rats represents a model of Parkinson's disease (PD). |
and alpha2-noradrenergic 81(1,1,1,1) | Details |
19580850 | Tantucci M, Mariucci G, Taha E, Spaccatini C, Tozzi A, Luchetti E, Calabresi P, Ambrosini MV: Induction of heat shock protein 70 reduces the alteration of striatal electrical activity caused by mitochondrial impairment. Biochem J. 1994 Jul 1;301 ( Pt 1):161-7. Corticostriatal slices from rats that had undergone mild thermal stress were exposed to either rotenone or 3-nitropropionic acid (3-NP), that selectively inhibits mitochondrial complex I and complex II, respectively. |
81(1,1,1,1) | Details |
18508033 | Chen YY, Chen G, Fan Z, Luo J, Ke ZJ: GSK3beta and endoplasmic reticulum stress mediate rotenone-induced death of SK-N-MC neuroblastoma cells. J Bioenerg Biomembr. 2005 Feb;37(1):1-15. Rotenone, an environmental toxin that inhibits mitochondrial complex I, has been used to induce experimental Parkinsonism in animals and cell cultures. |
81(1,1,1,1) | Details |
10477266 | Ferreirinha F, Duarte M, Melo AM, Videira A: Effects of disrupting the 21 kDa subunit of complex I from Neurospora crassa. Biochem J. 1999 Sep 15;342 Pt 3:551-4. Nevertheless, complex I of nuo21 is able to perform NADH:ubiquinone reductase activity, as judged by the observation that the respiration of mutant mitochondria is sensitive to inhibition by rotenone. |
36(0,1,1,6) | Details |
7823960 | Hofhaus G, Attardi G: Efficient selection and characterization of mutants of a human cell line which are defective in mitochondrial DNA-encoded subunits of respiratory NADH dehydrogenase. Biokhimiia. 1994 Nov;59(11):1638-45. In the course of analysis of eight mutants of the human cell line VA2B selected for their resistance to high concentrations of the complex I inhibitor rotenone, seven were found to be respiration deficient, and among these, six exhibited a specific defect of complex I. |
36(0,1,1,6) | Details |
16777535 | van der Merwe JA, Dubery IA: Benzothiadiazole inhibits mitochondrial NADH:ubiquinone oxidoreductase in tobacco. Neuropharmacology. 2007 Feb;52(2):536-41. Epub 2006 Oct 5. Using a dichlorodihydrofluorescein assay, it was found that benzothiadiazole, and the complex I inhibitor rotenone, increased reactive species production within cells in a concentration-dependent manner. |
34(0,1,1,4) | Details |
9309707 | Lenaz G, Bovina C, Castelluccio C, Fato R, Formiggini G, Genova ML, Marchetti M, Pich MM, Pallotti F, Parenti Castelli G, Biagini G: Mitochondrial complex I defects in aging. J Immunol. 2004 Dec 1;173(11):6973-80. In a study of Complex I activity in human platelet membranes we found that the enzyme activity was unchanged but the titre for half-inhibition by rotenone was significantly increased in aged individuals and proposed this change as a suitable biomarker of aging and age-related diseases. |
34(0,1,1,4) | Details |
15581661 | Alam M, Schmidt WJ: Mitochondrial complex I inhibition depletes plasma in the rotenone model of Parkinson's disease. J Biol Chem. 2008 Aug 22;283(34):23179-88. Epub 2008 Jun 18. In rats, rotenone, a mitochondrial complex I inhibitor, causes specific nigral dopaminergic neurodegeneration producing parkinsonian symptoms. |
32(0,1,1,2) | Details |
16965838 | Tretter L, Mayer-Takacs D, Adam-Vizi V: The effect of bovine serum albumin on the membrane potential and reactive species generation in -supported isolated brain mitochondria. Eur J Biochem. 1992 Sep 1;208(2):481-5. The high rate of H (2) O (2) generation measured in mitochondria prepared with digitonin (600.6+/-26.8pmol/min/mg protein) was inhibited by rotenone, consistently with a reverse flow of electrons via complex I. |
31(0,1,1,1) | Details |
15764812 | Singh SV, Srivastava SK, Choi S, Lew KL, Antosiewicz J, Xiao D, Zeng Y, Watkins SC, Johnson CS, Trump DL, Lee YJ, Xiao H, Herman-Antosiewicz A: prostate cancer cells is initiated by reactive species. J Appl Physiol. 1998 Feb;84(2):479-85. The SFN-induced ROS generation was significantly attenuated on pretreatment with mitochondrial respiratory chain complex I inhibitors, including diphenyleneiodonium and rotenone. |
-induced cell death in human 31(0,1,1,1) | Details |
19482916 | Giraud E, Van Aken O, Ho LH, Whelan J: The transcription factor ABI4 is a regulator of mitochondrial retrograde expression of ALTERNATIVE OXIDASE1a. Neurosci Lett. 2008 Nov 28;446(1):56-8. Epub 2008 Sep 11. This approach identified a strong repressor element, designated the B element, that was necessary for an increased promoter activity in response to the mitochondrial complex I inhibitor rotenone. |
31(0,1,1,1) | Details |
17442543 | Tan QR, Wang XZ, Wang CY, Liu XJ, Chen YC, Wang HH, Zhang RG, Zhen XC, Tong Y, Zhang ZJ: Differential effects of classical and atypical antipsychotic drugs on rotenone-induced neurotoxicity in PC12 cells. Sheng Li Xue Bao. 2007 Jun 25;59(3):253-9. In the present study, we compared the atypical agents, (RIP), (OLZ), and (QTP), with the classical agent haloperidol (HAL) in reducing cytotoxicity induced by rotenone, a mitochondrial complex I inhibitor, in PC12 cells. |
31(0,1,1,1) | Details |
15026259 | Bashkatova V, Alam M, Vanin A, Schmidt WJ: Chronic administration of rotenone increases levels of and lipid peroxidation products in rat brain. Eur Neuropsychopharmacol. 2007 Dec;17(12):768-73. Epub 2007 Apr 17. The complex I inhibitor rotenone is a neurotoxin that has been proposed to induce Parkinson-like degeneration. |
31(0,1,1,1) | Details |
10762085 | Seyfried J, Soldner F, Kunz WS, Schulz JB, Klockgether T, Kovar KA, Wullner U: Effect of 1-methyl-4-phenylpyridinium on pheochromocytoma PC 12 cells. Biochim Biophys Acta. 2008 May;1777(5):397-403. Epub 2008 Mar 18. Similarly, the complex I-inhibitor rotenone induced a time-dependent loss of GSH at 1 and 10 microM, whereas treatment with lower concentrations of rotenone (0.1, 0.01 microM) increased cellular GSH. |
in rat 31(0,1,1,1) | Details |
10378416 | Chen M, Andersen LP, Zhai L, Kharazmi A: Characterization of the respiratory chain of Helicobacter pylori. Biochim Biophys Acta. 1997 Apr 11;1319(2-3):223-32. The total insensitivity of activities of NADH dehydrogenase to rotenone and of -cytochrome c reductase to antimycin is indicative of the absence of the classical complex I of the electron transfer chain in this bacterium. |
31(0,1,1,1) | Details |
18053146 | Telang S, Lane AN, Nelson KK, Arumugam S, Chesney J: The oncoprotein H-RasV12 increases mitochondrial metabolism. . Pest Manag Sci. 2001 Oct;57(10):932-40. Importantly, ectopic expression of H-RasV12 sensitized immortalized cells to the ATP-depleting and cytotoxic effects of electron transport perturbation using the complex I inhibitor rotenone. |
31(0,1,1,1) | Details |
15806174 | Lee YJ, Lee DH, Cho CK, Chung HY, Bae S, Jhon GJ, Soh JW, Jeoung DI, Lee SJ, Lee YS: HSP25 inhibits radiation-induced apoptosis through reduction of PKCdelta-mediated ROS production. Arch Microbiol. 2008 Oct;190(4):471-80. Epub 2008 Jun 13. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. |
31(0,1,1,1) | Details |
15909418 | Tkachenko HM, Kurhaliuk NM, Vovkanych LS: [Effect of K-ATP channel opener-pinacidil on the liver mitochondria function in rats with different resistance to hypoxia during stress]. J Biol Chem. 1994 Jan 21;269(3):2263-9. The additional analyses were conducted with the use of inhibitors: mitochondrial enzyme complex I 10 mM rotenone and dehydrohenase 2 mM |
31(0,1,1,1) | Details |
18567707 | Gao Q, Wolin MS: Effects of hypoxia on relationships between cytosolic and mitochondrial NAD (P) H redox and generation in coronary arterial smooth muscle. FASEB J. 2006 Feb;20(2):259-68. Rotenone appeared to increase mitochondrial NAD (P) H and suggesting hypoxia could increase generation by complex I. |
6(0,0,1,1) | Details |
8986635 | Pitkanen S, Raha S, Robinson BH: Diagnosis of complex I deficiency in patients with lactic acidemia using skin fibroblast cultures. J Biol Chem. 1999 Jan 29;274(5):2625-30. Values for -cytochrome c reductase (rotenone sensitive) were compared for a series of three controls and nine patients with complex I (NADH-coenzyme Q reductase deficiency). |
6(0,0,1,1) | Details |
16725203 | Kou J, Klorig DC, Bloomquist JR: Potentiating effect of the ATP-sensitive potassium channel blocker glibenclamide on complex I inhibitor neurotoxicity in vitro and in vivo. Biochem J. 2006 Apr 15;395(2):405-15. We measured the ability of mitochondrial inhibitors of complexes I (rotenone, MPP (+), and HPP (+)), II (amdro), IV (Na and an uncoupler (dinoseb) to release preloaded from murine striatal synaptosomes. |
4(0,0,0,4) | Details |
9119899 | Kilbourn MR, Charalambous A, Frey KA, Sherman P, Higgins DS Jr, Greenamyre JT: Intrastriatal neurotoxin injections reduce in vitro and in vivo binding of radiolabeled rotenoids to mitochondrial complex I. Ann Neurol. 1988 Mar;23(3):287-94. |
4(0,0,0,4) | Details |
18140 | Ragan CI, Bloxham DP: Specific labelling of a constituent polypeptide of bovine heart mitochondrial -ubiquinone reductase by the inhibitor diphenyleneiodonium. J Neurol Sci. 1987 Apr;78(2):189-201. Rotenone increased the apparent affinity of diphenyleneiodonium for the 23500-mol.wt. polypeptide without affecting the maximum incorporation. 8. -ubiquinone-1 and -menadione reductase activities of Complex I were inhibited by diphenyleneiodonium (apparent Ki 23 and 30 nmol/mg of protein respectively). |
3(0,0,0,3) | Details |
9707444 | Bai Y, Attardi G: The mtDNA-encoded ND6 subunit of mitochondrial NADH dehydrogenase is essential for the assembly of the membrane arm and the respiratory function of the enzyme. Neurochem Res. 2009 Jun 4. Seven of the approximately 40 subunits of the mammalian respiratory NADH dehydrogenase (Complex I) are encoded in mitochondrial DNA (mtDNA). |
2(0,0,0,2) | Details |
7797367 | Fukushima T, Isobe A, Joho N, Shiwaku K, Yamane Y, Torii M: The fatty acids of each lipid fraction and their use in providing energy source of the plerocercoid of Spirometra erinacei. Int J Parasitol. 1991 Dec;21(8):965-8. Michaelis constants (Km) of beta-hydroxyacyl-CoA dehydrogenase (HAD), oxidoreductase (complex I) ferricyanide reaction) and complex I reaction) for were 20.6, 50 and 13.3 microM, respectively. The ATP production in mitochondria of the plerocercoids was accelerated by adding ADP and inhibited by adding such electron transport system inhibitors as rotenone, antimycin A and |
2(0,0,0,2) | Details |
9831004 | Pezzi PP, De Negri AM, Sadun F, Carelli V, Leuzzi V: Childhood Leber's hereditary optic neuropathy (ND1/3460) with visual recovery. J Neurosci Res. 2007 Nov 15;85(15):3471-9. The specific activity of complex I in platelets was reduced in the proband and normal in his relatives. An abnormal resistance of NADH:ubiquinone reductase to the inhibitory effect of rotenone was found in platelet mitochondria from the proband and family members and was consistent with the degree of heteroplasmy. |
2(0,0,0,2) | Details |
9155526 | Cornelissen J, Van Kuilenburg AB, Voute PA, Van Gennip AH: The effect of the neuroblastoma-seeking agent meta-iodobenzylguanidine (MIBG) on -driven formation and -driven lipid peroxidation in beef heart submitochondrial particles. Cytometry A. 2010 Apr;77(4):310-20. MIBG is a structural analogue of and is capable of inhibiting complex I and complex III of the respiratory chain. The effect of MIBG is comparable to that of rotenone (an inhibitor of complex I) rather than that of antimycin (an inhibitor of complex III). |
2(0,0,0,2) | Details |
16292513 | Lee SJ, Youn YC, Han ES, Lee CS: Depressant effect of mitochondrial respiratory complex inhibitors on proteasome inhibitor-induced mitochondrial dysfunction and cell death in PC12 cells. J Biol Chem. 2005 Dec 30;280(52):42655-68. Epub 2005 Oct 19. The addition of rotenone (inhibitor of respiratory complex I), 3-nitropropionic acid (complex II inhibitor), harmine (inhibitor of complexes I and II) and cyclosporin A (CsA, an inhibitor of the mitochondrial permeability transition) reduced the nuclear damage, loss in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive species and depletion of in differentiated PC12 cells treated with MG132, a proteasome inhibitor. The addition of rotenone (inhibitor of respiratory complex I), 3-nitropropionic acid (complex II inhibitor), harmine (inhibitor of complexes I and II) and cyclosporin A (CsA, an inhibitor of the mitochondrial permeability transition) reduced the nuclear damage, loss in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive species and depletion of in differentiated PC12 cells treated with MG132, a proteasome inhibitor. |
2(0,0,0,2) | Details |
19577342 | Caro P, Gomez J, Sanchez I, Lopez-Torres M, Barja G: [Effect of restricting amino acids except ROS production in isolated liver mitochondria was unchanged with complex I / or / or complex II linked substrates. |
on mitochondrial oxidative stress]. J Pharmacol Exp Ther. 2004 Dec;311(3):948-53. Epub 2004 Jul 27.1(0,0,0,1) | Details |
15451049 | Bretaud S, Lee S, Guo S: Sensitivity of zebrafish to environmental toxins implicated in Parkinson's disease. Comp Biochem Physiol A Mol Integr Physiol. 2002 May;132(1):107-9. One valuable type of animal model for PD is established by treating animals with PD-inducing neurotoxins, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat. These neurotoxins are thought to inhibit mitochondrial complex I activity leading to oxidative stress, impaired energy metabolism, proteasomal dysfunction, and, eventually, neuronal loss. |
1(0,0,0,1) | Details |
39543 | Takeshige K, Minakami S: heart submitochondrial particles and -ubiquinone reductase preparation. J Neurochem. 2000 Dec;75(6):2611-21. The effects of pH and inorganic salts at high concentrations on the - and -dependent reactions of Complex I were essentially similar to those on the reactions of submitochondrial particles. 3. The reaction was inhibited by treatment of the preparation with p-hydroxymercuribenzoate and stimulated by treatment with rotenone. |
- and -dependent formation of anions by bovine 1(0,0,0,1) | Details |
494059 | Breen GA, Scheffler IE: Respiration-deficient Chinese hamster cell mutants: biochemical characterization. Somatic Cell Genet. 1979 Jul;5(4):441-51. We show that these mutants all have a defect in complex I of the electron-transport chain. The general features of these mutants are: (1) a low rate of O2 consumption in whole cells; (2) a low rate of release of 14CO2 from [2-14C] [1-14C] and [3-14C] (3) a low rate of release of 14CO2 from [5-14C] and [1-14C] in mutants from groups II, VII, and the "overlapping" mutant, whereas a significant amount of 14CO2 is released in mutants from group I; (4) a substantial rate of release of 14CO2 from [U-14C] asparate; (5) in isolated mitochondria, and alpha- stimulate O2 consumption whereas substrates which generate such as do not; and (6) there is little or no rotenone-sensitive oxidase activity in isolated mitochondria. |
1(0,0,0,1) | Details |
10917650 | Lummen P: Biochemical aspects of N-heterocyclic complex-I inhibitors with insecticidal activity. Biochem Soc Trans. 1999 Aug;27(4):602-6. |
1(0,0,0,1) | Details |
7476924 | van de Water B, Zoeteweij JP, de Bont HJ, Nagelkerke JF: Inhibition of succinate:ubiquinone reductase and decrease of in nephrotoxic S-conjugate-induced oxidative cell injury. Brain Res. 2004 Jul 23;1015(1-2):73-81. KCN cytoprotection could be prevented by inhibition of SQR activity with or TTFA, whereas inhibition of either complex I or III with rotenone and antimycin, respectively, did not prevent it. The DCVC-induced oxidative stress was associated with a decrease in the succinate:ubiquinone reductase (SQR) activity of complex II, whereas NADH:ubiquinone reductase activity of complex I remained unaffected. |
1(0,0,0,1) | Details |
15280438 | Watabe M, Nakaki T: Rotenone induces apoptosis via activation of bad in human dopaminergic SH-SY5Y cells. J Neurosci. 2007 Jul 4;27(27):7310-7. Chronic complex I inhibition caused by rotenone induces features of Parkinson's disease in rats, including selective nigrostriatal dopaminergic degeneration and Lewy bodies with alpha-synuclein-positive inclusions. |
81(1,1,1,1) | Details |
8638946 | Tein I, Bukovac SW, Xie ZW: Characterization of the human plasmalemmal transporter in cultured skin fibroblasts. J Neurosci Res. 2002 Aug 15;69(4):559-66. The effects of different site-specific respiratory chain toxins, namely, rotenone (complex I), antimycin A (complex III), and (KCN) (complex IV) on uptake was also examined. |
81(1,1,1,1) | Details |
15215104 | Mills SD, Yang W, MacCormack K: Molecular characterization of benzimidazole resistance in Helicobacter pylori. Antimicrob Agents Chemother. 2004 Jul;48(7):2524-30. MIC testing of the wild-type H. pylori strain and four classes of nuo mutants revealed that all NuoD mutant classes were hypersensitive to rotenone, a known inhibitor of complex I (NADH:ubiquinone oxidoreductase) suggested to bind to NuoD. |
81(1,1,1,1) | Details |
16115719 | Hirata Y, Nagatsu T: Rotenone and CCCP inhibit hydroxylation in rat striatal tissue slices. Biochem Pharmacol. 2008 Jul 1;76(1):128-38. Epub 2008 Apr 29. Complex I inhibition has been implicated in the neurotoxicity of MPTP and rotenone, which reproduce a neurochemical and neuropathological feature of Parkinson's disease in experimental animals. |
81(1,1,1,1) | Details |
9199966 | Katsikis PD, Garcia-Ojeda ME, Torres-Roca JF, Greenwald DR, Herzenberg LA, Herzenberg LA: HIV type 1 Tat protein enhances activation-but not Fas (CD95)-induced peripheral blood T cell apoptosis in healthy individuals. Toxicon. 2003 Sep 15;42(4):351-7. Examining the mechanisms by which Tat induces apoptosis, we found that inhibitors of reactive intermediate (ROI) generation or neutralizers of ROI, such as rotenone, a potent inhibitor of mitochondrial complex I of the respiratory chain, and 3,3,5,5-tetramethylpyrroline N-oxide (TMPO), an electron spin trap, could both enhance the spontaneous apoptosis induced by Tat. |
81(1,1,1,1) | Details |
19088429 | Oliver R 3rd, Friday E, Turturro F, Welbourne T: Troglitazone induced cytosolic acidification via extracellular signal-response kinase activation and mitochondrial depolarization: complex I pumping regulates ammoniagenesis in proximal tubule-like LLC-PK1 cells. Biol Pharm Bull. 1999 Mar;22(3):240-3. TRO-enhanced acid production was correlated with mitochondrial membrane potential and rotenone and 5-(N-ethyl-N-isopropyl) amiloride, were employed to test specifically the role of Complex I pumping. |
36(0,1,1,6) | Details |
17038483 | Richardson JR, Caudle WM, Guillot TS, Watson JL, Nakamaru-Ogiso E, Seo BB, Sherer TB, Greenamyre JT, Yagi T, Matsuno-Yagi A, Miller GW: Obligatory role for complex I inhibition in the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9893-8. Recently, we reported that the yeast single-subunit nicotinamide adenine dinucleotide (reduced) dehydrogenase (NDI1) is resistant to rotenone, a complex I inhibitor that produces a parkinsonian syndrome in rats, and that overexpression of NDI1 in SK-N-MC cells prevents the toxicity of rotenone. |
36(0,1,1,6) | Details |
12180906 | Kushnareva Y, Murphy AN, Andreyev A: Complex I-mediated reactive species generation: modulation by cytochrome c and NAD (P)+ oxidation-reduction state. Exp Cell Res. 1999 Jun 15;249(2):396-403. This increased ROS production can be mimicked by rotenone, a complex I inhibitor, as well as other chemical inhibitors of electron flow that act further downstream in the electron transport chain. |
34(0,1,1,4) | Details |
12911637 | Hoglinger GU, Carrard G, Michel PP, Medja F, Lombes A, Ruberg M, Friguet B, Hirsch EC: Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease. J Physiol. 2002 Nov 1;544(Pt 3):687-93. Proteasome inhibition potentiated the toxicity of rotenone, MPP+ and at concentrations at which they increased free radical levels >/= 40% above baseline, exceeding the cellular capacity to detoxify oxidized proteins reduced by proteasome inhibition, and also exacerbated ATP depletion caused by complex I inhibition. |
34(0,1,1,4) | Details |
1900156 | Anderson WM, Chambers BB, Wood JM, Benninger L: Inhibitory effects of two structurally related carbocyanine laser dyes on the activity of bovine heart mitochondrial and Paracoccus denitrificans -ubiquinone reductase. Novartis Found Symp. 2006;272:54-64; discussion 64-72 The mechanism of inhibition (except for the HIDC effect on reduction with P. denitrificans) appeared to be through the interaction of dye with the rotenone site on -ubiquinone reductase (EC 1.6.99.3), since rotenone-insensitive preparations of complex I and P. denitrificans membrane vesicles were also insensitive to HIDC and HITC inhibition. |
33(0,1,1,3) | Details |
7931358 | Hartley A, Stone JM, Heron C, Cooper JM, Schapira AH: Complex I inhibitors induce dose-dependent apoptosis in PC12 cells: relevance to Parkinson's disease. J Biol Chem. 2010 Jan 15;285(3):2040-50. Epub 2009 Nov 4. We have investigated the mode of death induced by complex I inhibition of dopaminergic cell cultures, and our results suggest that both 1-methyl-4-phenylpyridinium and rotenone cause apoptosis at low concentrations and necrosis at high concentrations. |
32(0,1,1,2) | Details |
11078378 | Yuki K, Miyauchi T, Kakinuma Y, Murakoshi N, Suzuki T, Hayashi J, Goto K, Yamaguchi I: Mitochondrial dysfunction increases expression of endothelin-1 and induces apoptosis through caspase-3 activation in rat cardiomyocytes in vitro. J Neurochem. 2002 Jul;82(1):66-74. Therefore, in order to elucidate this problem, we developed an in vitro model of mitochondrial dysfunction using rotenone, a mitochondrial respiratory chain complex I inhibitor, and studied preproendothelin-1 gene expression and apoptosis. |
31(0,1,1,1) | Details |
17176833 | Bondarenko OI, Sahach VF: [Role of mitochondria in reglulation of endothelial cell hyperpolarization to Fiziol Zh. 2006;52(5):6-11. Protonofore CCCP and rotenone, an electron transport chain complex I inhibitor, agents that cause mitochondria depolarization, inhibited the sustained hyperpolarization of endothelial cells. |
31(0,1,1,1) | Details |
16686432 | Nurse CA, Buttigieg J, Thompson R, Zhang M, Cutz E: For example, the complex I blocker, rotenone (1 microM), mimics hypoxia in causing K+ channel inhibition and ATP secretion, and occludes hypoxic sensitivity. |
sensing in neuroepithelial and chromaffin cells. Novartis Found Symp. 2006;272:106-14; discussion 114-831(0,1,1,1) | Details |
10514095 | Duan W, Zhang Z, Gash DM, Mattson MP: Participation of prostate apoptosis response-4 in degeneration of dopaminergic neurons in models of Parkinson's disease. Exp Lung Res. 2002 Jul-Aug;28(5):373-89. Exposure of cultured human dopaminergic neural cells to the complex I inhibitor rotenone, or to Fe2+, resulted in Par-4 induction, mitochondrial dysfunction, and subsequent apoptosis. |
31(0,1,1,1) | Details |
18486118 | Rojas JC, Saavedra JA, Gonzalez-Lima F: Neuroprotective effects of memantine in a mouse model of retinal degeneration induced by rotenone. Biochem J. 2002 Dec 1;368(Pt 2):545-53. We tested the hypothesis that uncompetitive NMDAR blockade with memantine prevents mitochondrial dysfunction-related neurodegeneration in vivo, using a mouse model of retinal ganglion cell layer (GCL) degeneration induced by rotenone, a mitochondrial complex I inhibitor. |
31(0,1,1,1) | Details |
10908611 | Luetjens CM, Bui NT, Sengpiel B, Munstermann G, Poppe M, Krohn AJ, Bauerbach E, Krieglstein J, Prehn JH: Delayed mitochondrial dysfunction in excitotoxic neuron death: cytochrome c release and a secondary increase in production. Mol Cancer. 2007 Dec 1;6:77. The secondary rise could be inhibited by the complex I inhibitor rotenone (in combination with oligomycin) and mimicked by the complex III inhibitor antimycin A. |
31(0,1,1,1) | Details |
17581813 | Marella M, Seo BB, Matsuno-Yagi A, Yagi T: Mechanism of cell death caused by complex I defects in a rat dopaminergic cell line. Can J Microbiol. 2005 Aug;51(8):695-703. We have shown that expression of a rotenone-insensitive yeast -quinone oxidoreductase (Ndi1) can rescue mammalian cells from complex I dysfunction. |
18(0,0,2,8) | Details |
17332151 | Janssen AJ, Trijbels FJ, Sengers RC, Smeitink JA, van den Heuvel LP, Wintjes LT, Stoltenborg-Hogenkamp BJ, Rodenburg RJ: Spectrophotometric assay for complex I of the respiratory chain in tissue samples and cultured fibroblasts. Brain Res. 2005 Jul 27;1051(1-2):25-34. CONCLUSIONS: This spectrophotometric assay is reproducible, sensitive, and specific for complex I activity because of its high rotenone sensitivity, and it can be applied successfully to the diagnosis of complex I deficiencies. |
13(0,0,1,8) | Details |
9377792 | Ribeiro SM, Campello AP, Nascimento AJ, Kluppel ML: Effect of amiodarone (AMD) on the antioxidant enzymes, lipid peroxidation and mitochondrial metabolism. Cell Biochem Funct. 1997 Sep;15(3):145-52. The results confirm the effects of AMD on complex I and permit the placing of this drug in class A of the classification of Knobeloch, together with rotenone, amytal and chaotropic agents. |
6(0,0,1,1) | Details |
9625705 | Bernhard Teicher H, Vibe Scheller H: The NAD (P) H dehydrogenase in barley thylakoids is photoactivatable and uses The enzyme was sensitive to rotenone, confirming the involvement of a complex I-type enzyme. |
as well as . Plant Physiol. 1998 Jun;117(2):525-32.6(0,0,1,1) | Details |
9914819 | Lenaz G, Cavazzoni M, Genova ML, D'Aurelio M, Merlo Pich M, Pallotti F, Formiggini G, Marchetti M, Parenti Castelli G, Bovina C: Oxidative stress, antioxidant defences and aging. Biochemistry. 2009 Jan;74(1):47-53. Complex I activity and its rotenone sensitivity decreased in brain cortex non-synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. |
6(0,0,1,1) | Details |
6513990 | Takamiya S, Furushima R, Oya H: Electron transfer complexes of Ascaris suum muscle mitochondria: I. Mol Pharmacol. 1995 Nov;48(5):825-34. Characterization of -cytochrome c reductase (complex I-III), with special reference to cytochrome localization.. The enzyme preparation catalyzed the reduction of 1.68 mumol cytochrome c min-1 mg-1 protein at 25 degrees C with but not with and retained its sensitivity to rotenone, piericidin A and 2-heptyl-4-hydroxyquinoline-N-oxide as with the submitochondrial particles. |
4(0,0,0,4) | Details |
10491161 | Almeida T, Duarte M, Melo AM, Videira A: The 24-kDa iron-complex I is required for enzyme activity. Oncogene. 1999 Nov 4;18(46):6380-7. In agreement with this, the respiration of intact mitochondria or mitochondrial membranes from the mutant strain is insensitive to rotenone inhibition. |
subunit of 4(0,0,0,4) | Details |
18485875 | Martinvalet D, Dykxhoorn DM, Ferrini R, Lieberman J: Granzyme A cleaves a mitochondrial complex I protein to initiate caspase-independent cell death. Cell. 2008 May 16;133(4):681-92. |
2(0,0,0,2) | Details |
16919272 | Centonze D, Prosperetti C, Barone I, Rossi S, Picconi B, Tscherter A, De Chiara V, Bernardi G, Calabresi P: NR2B-containing NMDA receptors promote the effects of 3-nitropropionic acid but not of rotenone in the striatum. Exp Neurol. 2006 Dec;202(2):470-9. Epub 2006 Aug 17. Decreased activity of mitochondrial complex I and II is implicated in the pathophysiology of progressive supranuclear palsy (PSP) and Huntington's disease (HD), respectively. |
2(0,0,0,2) | Details |
17583437 | Behrouz B, Drolet RE, Sayed ZA, Lookingland KJ, Goudreau JL: Unique responses to mitochondrial complex I inhibition in tuberoinfundibular neurons may impart resistance to toxic insult. J Biol Chem. 2005 Apr 22;280(16):15587-94. Epub 2005 Feb 14. In the present experiments, direct exposure to rotenone or 1-methyl-4-phenylpyridinium (MPP+) had no effect on mediobasal hypothalamic TIDA neurons, but significantly increased the percentage of apoptag immunoreactive neurons in midbrain primary NSDA and MLDA cultures. |
2(0,0,0,2) | Details |
1907569 | Berger S, Ellersiek U, Steinmuller K: Cyanobacteria contain a mitochondrial complex I-homologous NADH-dehydrogenase. Toxicol Sci. 2009 Dec;112(2):427-34. Epub 2009 Sep 18. Both membranes oxidize in a rotenone-sensitive reaction. |
2(0,0,0,2) | Details |
2174736 | Modica-Napolitano JS, Joyal JL, Ara G, Oseroff AR, Aprille JR: Mitochondrial toxicity of cationic photosensitizers for photochemotherapy. Neurology. 1997 Jun;48(6):1623-32. With photoirradiation VB-BO was also shown to inhibit rotenone-sensitive -cytochrome c reductase activity, but it had no effect on -cytochrome c reductase activity. These data indicate that photoactivation of VB-BO produces selective inhibition of mitochondrial respiratory complex I. |
2(0,0,0,2) | Details |
19250966 | Mastroberardino PG, Hoffman EK, Horowitz MP, Betarbet R, Taylor G, Cheng D, Na HM, Gutekunst CA, Gearing M, Trojanowski JQ, Anderson M, Chu CT, Peng J, Greenamyre JT: A novel transferrin/TfR2-mediated mitochondrial iron transport system is disrupted in Parkinson's disease. Neurobiol Dis. 2009 Jun;34(3):417-31. Epub 2009 Feb 26. Importantly, the Tf/TfR2 pathway can deliver Tf bound iron to mitochondria and to the respiratory complex I as well. In the rotenone model of PD, Tf accumulates in neurons, with much of it accumulating in the mitochondria. |
1(0,0,0,1) | Details |
12399275 | Madapallimattam AG, Law L, Jeejeebhoy KN: Effect of hypoenergetic feeding on muscle oxidative phosphorylation and mitochondrial complex I-IV activities in rats. Antioxid Redox Signal. 2007 Nov;9(11):1825-36. RESULTS: A significant relation was observed between weight loss and the state 4 and 3 oxidation rates with + and for state 3 + and + rotenone but not with tetramethyl-p-phenylenediamine + + antimycin A (TMPD). |
1(0,0,0,1) | Details |
16416317 | Igamberdiev AU, Shen T, Gardestrom P: Function of mitochondria during the transition of barley protoplasts from low light to high light. Biochim Biophys Acta. 1999 May 26;1412(1):56-65. Rotenone (an inhibitor of mitochondrial complex I) had similar, but less pronounced effect as oligomycin. Rotenone (an inhibitor of mitochondrial complex I) had similar, but less pronounced effect as oligomycin. |
1(0,0,0,1) | Details |
1497658 | Sivan VM, Raj RK: mitochondria-like particles from Setaria digitata, a filarial parasite. Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):826-33. Epub 2008 Apr 18. In the cattle filarial parasite, Setaria digitata, the mitochondria-like particles have been shown to possess site I associated oxidative phosphorylation and rotenone sensitive and insensitive pathways for the dehydrogenation of Thus activities of complex I and reductase are linked to |
dependent dehydrogenation in 1(0,0,0,1) | Details |
17291988 | Wang QS, Zheng YM, Dong L, Ho YS, Guo Z, Wang YX: Role of mitochondrial reactive hypoxia-dependent increase in intracellular in pulmonary artery myocytes. Sheng Li Xue Bao. 2006 Oct 25;58(5):421-8. Here we report that in freshly isolated mouse PASMCs, which are devoid of the mixed responses from multi-types of cells in lungs and significant changes in gene expression in cultured cells, the mitochondrial electron transport chain (ETC) complex I, II, or III inhibitors blocked hypoxia-induced increases in intracellular ROS and Ca2+ concentration ([ROS] i and [Ca2+] i) without effects on their resting levels. Moreover, H2O2 (5.1 microM) reversed the inhibition of the hypoxia-induced increase in [Ca2+] i by rotenone. |
species in 1(0,0,0,1) | Details |
19860724 | Agnati FL, Guidolin D, Baluska F, Leo G, Barlow PW, Carone C, Genedani S: A New Hypothesis of Pathogenesis Based on the Divorce between Mitochondria and their Host Cells: Possible Relevances for the Alzheimer's Disease. Bioorg Med Chem Lett. 2009 Feb 1;19(3):972-5. Epub 2008 Nov 24. As a matter of fact, alpha-syn can enter mitochondria and interact with complex I causing respiratory deficiency and increased free radical production. This proposal finds indirect support from observations on rotenone-poisoned glioblastoma cells which have been co-cultured with non-poisoned cells. |
1(0,0,0,1) | Details |
19114648 | Chan SH, Wu KL, Chang AY, Tai MH, Chan JY: Oxidative impairment of mitochondrial electron transport chain complexes in rostral ventrolateral medulla contributes to neurogenic hypertension. Hypertension. 2009 Feb;53(2):217-27. Epub 2008 Dec 29. This mobile electron carrier also antagonized the elevated H (2) O (2) in RVLM and vasopressor responses to complex I (rotenone) or III (antimycin A) inhibitor in Wistar-Kyoto or prehypertensive rats. |
81(1,1,1,1) | Details |
16667685 | Pascal N, Dumas R, Douce R: Comparison of the Kinetic Behavior toward Linked Dehydrogenases from Plant Mitochondria. Biofizika. 2000 Jul-Aug;45(4):695-9. It is suggested that (+)-linked malic enzyme, when fully activated, is able to raise the matricial level up to the required concentration to fully engage the rotenone-resistant internal NADH-dehydrogenase, whose affinity for is weaker than complex I. |
Nucleotides of -81(1,1,1,1) | Details |
11431129 | Schuchmann S, Kovacs R, Kann O, Heinemann U, Buchheim K: Monitoring NAD (P) H autofluorescence to assess mitochondrial metabolic functions in rat hippocampal-entorhinal cortex slices. Behav Brain Res. 2004 Aug 31;153(2):439-46. In contrast, the increase in NAD (P) H signal that followed a brief inhibition of mitochondrial respiratory chain complex I using rotenone (1 microM) indicated an accumulation of NAD (P) H. |
81(1,1,1,1) | Details |
15845907 | Basta G, Lazzerini G, Del Turco S, Ratto GM, Schmidt AM, De Caterina R: At least 2 distinct pathways generating reactive mediate vascular cell adhesion molecule-1 induction by advanced glycation end products. Toxicol Appl Pharmacol. 1997 Jul;145(1):74-81. The inhibition of NAD (P) H oxidase by apocynin and diphenylene iodonium, and of the mitochondrial electron transport system at complex II by thenoyltrifluoroacetone (TTFA), significantly inhibited both AGE-induced ROS production and VCAM-1 expression, whereas these effects were potentiated by rotenone and antimycin A, specific inhibitors of mitochondrial complex I and III, respectively. |
species 81(1,1,1,1) | Details |
20117074 | Tocilescu MA, Fendel U, Zwicker K, Drose S, Kerscher S, Brandt U: The role of a conserved complex I for binding and reduction. Biochim Biophys Acta. 2010 Feb 1. Apparent K (m) values for Q (1) and Q (2) were markedly increased and we found pronounced resistance to the complex I inhibitors decyl-quinazoline-amine (DQA) and rotenone. |
in the 49-kDa subunit of 36(0,1,1,6) | Details |
12231169 | Seo BB, Nakamaru-Ogiso E, Flotte TR, Yagi T, Matsuno-Yagi A: A single-subunit quinone oxidoreductase renders resistance to mammalian nerve cells against complex I inhibition. Mol Gen Genet. 1996 Aug 27;252(1-2):177-83. The cells expressing the Ndi1 protein were resistant to known inhibitors of complex I, such as rotenone and pyridaben. |
-36(0,1,1,6) | Details |
7503762 | Wyatt KM, Skene C, Veitch K, Hue L, McCormack JG: The antianginal agent ranolazine is a weak inhibitor of the respiratory complex I, but with greater potency in broken or uncoupled than in coupled mitochondria. Biochem Pharmacol. 1995 Nov 9;50(10):1599-606. Studies with different electron acceptors and respiratory inhibitors indicated that it inhibits respiratory Complex I at a site between ferricyanide and and reduction (i.e. at a similar locus to rotenone). |
33(0,1,1,3) | Details |
11689167 | King TD, Bijur GN, Jope RS: Caspase-3 activation induced by inhibition of mitochondrial complex I is facilitated by glycogen synthase kinase-3beta and attenuated by lithium. Arch Biochem Biophys. 1996 May 15;329(2):145-55. To test if these regulatory interactions applied to other mitochondrial complex I inhibitors, cells were treated with rotenone. |
33(0,1,1,3) | Details |
14715437 | Xu G, Perez-Pinzon MA, Sick TJ: Mitochondrial complex I inhibition produces selective damage to hippocampal subfield CA1 in organotypic slice cultures. Neurotox Res. 2003;5(7):529-38. Slice cultures, 2-3 week old, were exposed for 1 h to either the Complex I inhibitors, rotenone or 1-methyl-4-phenylpyridium (MPP+), the Complex II inhibitor 3-nitropropionic acid (3-NP), or the excitotoxin |
32(0,1,1,2) | Details |
12437580 | Wang X, Qin ZH, Leng Y, Wang Y, Jin X, Chase TN, Bennett MC: inhibits rotenone-induced apoptosis in SH-SY5Y cells. J Neurosci. 2003 Nov 26;23(34):10756-64. To elucidate molecular mechanisms possibly linking these events, as well as to evaluate the neuroprotective potential of the cyclopentenone an inducer of heat shock proteins (HSPs), we exposed human dopaminergic SH-SY5Y cells to the complex I inhibitor rotenone. |
32(0,1,1,2) | Details |
9225812 | Fujibayashi Y, Taniuchi H, Yonekura Y, Ohtani H, Konishi J, Yokoyama A: hypoxia imaging agent with high membrane permeability and low redox potential. J Biol Chem. 1986 Mar 5;261(7):3068-74. As a model of hypoxic mitochondria, rotenone (Complex I inhibitor)-treated mitochondria were used. |
-62-ATSM: a new 31(0,1,1,1) | Details |
14743397 | Shih CM, Ko WC, Wu JS, Wei YH, Wang LF, Chang EE, Lo TY, Cheng HH, Chen CT: Mediating of caspase-independent apoptosis by cadmium through the mitochondria-ROS pathway in MRC-5 fibroblasts. Curr Neuropharmacol. 2006 Jan;4(1):69-75. Using inhibitors of the mitochondrial electron transport chain (ETC) (oligomycin A and rotenone for complex I and V, respectively) and mitochondrial permeability transition pore (MPTP) (cyclosporin A and aristolochic acid), we coincidently found the ROS production, mitochondrial membrane depolarization, and apoptotic content were almost completely or partially abolished. |
31(0,1,1,1) | Details |
18522491 | Wenzel P, Mollnau H, Oelze M, Schulz E, Wickramanayake JM, Muller J, Schuhmacher S, Hortmann M, Baldus S, Gori T, Brandes RP, Munzel T, Daiber A: First evidence for a crosstalk between mitochondrial and nitroglycerin-triggered vascular dysfunction. Clin Chim Acta. 2006 Dec;374(1-2):81-6. Epub 2006 Jun 2. Vice versa, tolerance was attenuated by co-treatment with the respiratory chain complex I inhibitor rotenone (100 microg/h/4 day) or the mitochondrial permeability transition pore blocker cyclosporine A (50 microg/h/4 day). |
oxidase-derived reactive species in 31(0,1,1,1) | Details |
14550906 | Orth M, Tabrizi SJ, Schapira AH, Cooper JM: Alpha-synuclein expression in HEK293 cells enhances the mitochondrial sensitivity to rotenone. J Biol Chem. 2005 Jul 15;280(28):25994-6001. Epub 2005 Apr 22. However, both wild-type and mutant G209A alpha-synuclein expression enhanced the fall in mitochondrial membrane potential induced by the complex I inhibitor rotenone. |
31(0,1,1,1) | Details |
7566122 | Jouaville LS, Ichas F, Holmuhamedov EL, Camacho P, Lechleiter JD: Synchronization of substrates in Xenopus laevis oocytes. J Neurosci. 2005 Oct 26;25(43):10029-40. The effects of / are blocked by ruthenium red at the Ca2+ uniporter, by rotenone at complex I, and by antimycin A at complex III, and are subsequently rescued at complex IV by tetramethylphenylenediamine (TMPD). |
waves by mitochondrial 31(0,1,1,1) | Details |
10597238 | Suzuki S, Higuchi M, Proske RJ, Oridate N, Hong WK, Lotan R: Implication of mitochondria-derived reactive species, cytochrome C and caspase-3 in N-(4-hydroxyphenyl) retinamide-induced apoptosis in cervical carcinoma cells. J Biol Chem. 1996 Jun 21;271(25):14785-90. Rotenone, an MRC complex I inhibitor was less effective and azide, an MRC complex IV inhibitor, exhibited a marginal effect. |
31(0,1,1,1) | Details |
9689052 | Seo BB, Kitajima-Ihara T, Chan EK, Scheffler IE, Matsuno-Yagi A, Yagi T: Molecular remedy of complex I defects: rotenone-insensitive internal -quinone oxidoreductase of Saccharomyces cerevisiae mitochondria restores the oxidase activity of complex I-deficient mammalian cells. Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9167-71. |
12(0,0,2,2) | Details |
15849190 | Pineau B, Mathieu C, Gerard-Hirne C, De Paepe R, Chetrit P: Targeting the NAD7 subunit to mitochondria restores a functional complex I and a wild type phenotype in the Nicotiana sylvestris CMS II mutant lacking nad7. Physiol Plant. 2007 Dec;131(4):527-41. CMSII plants lack rotenone-sensitive complex I activity and are impaired in physiological and phenotypical traits. |
12(0,0,1,7) | Details |
15450959 | Cardol P, Vanrobaeys F, Devreese B, Van Beeumen J, Matagne RF, Remacle C: Higher plant-like subunit composition of mitochondrial complex I from Chlamydomonas reinhardtii: 31 conserved components among eukaryotes. Neurosci Lett. 2002 Jun 28;326(2):97-100. The rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) is the most intricate membrane-bound enzyme of the mitochondrial respiratory chain. |
12(0,0,1,7) | Details |
18957561 | de Wit LE, Scholte HR, Sluiter W: Correct assay of complex I activity in human skin fibroblasts by timely addition of rotenone. Clin Chem. 2008 Nov;54(11):1921-2; author reply 1922-4. |
6(0,0,1,1) | Details |
16828729 | Benit P, Goncalves S, Philippe Dassa E, Briere JJ, Martin G, Rustin P: Three spectrophotometric assays for the measurement of the five respiratory chain complexes in minuscule biological samples. Genetics. 2001 Jul;158(3):1051-60. A third assay measures rotenone-sensitive complex I activity and subsequently oligomycin-sensitive complex V activity. |
6(0,0,1,1) | Details |
8546703 | Degli Esposti M, Ngo A, McMullen GL, Ghelli A, Sparla F, Benelli B, Ratta M, Linnane AW: The specificity of mitochondrial complex I for ubiquinones. J Cell Biochem. 2000 Oct 20;80(2):216-22. The rate of NADH:Q reductase activity is potently but incompletely inhibited by rotenone, and the residual rotenone-insensitive rate is stimulated by Q analogues in different ways depending on the hydrophobicity of their substituent. |
6(0,0,0,6) | Details |
19047048 | Porcelli AM, Angelin A, Ghelli A, Mariani E, Martinuzzi A, Carelli V, Petronilli V, Bernardi P, Rugolo M: Respiratory complex I dysfunction due to mitochondrial DNA mutations shifts the voltage threshold for opening of the permeability transition pore toward resting levels. Eur J Pharmacol. 1995 Jul 14;280(3):251-6. The addition of rotenone to HL180 cells and of antimycin A to XTC.UC1 cells caused fast mitochondrial membrane depolarization that was prevented by treatment with cyclosporin A, intracellular Ca2+ chelators, and antioxidant. |
4(0,0,0,4) | Details |
19433311 | Plecita-Hlavata L, Jezek J, Jezek P: Pro-oxidant mitochondrial matrix-targeted MitoQ10 acts as anti-oxidant at retarded electron transport or pumping within Complex I. Neurosci Lett. 2006 Apr 10-17;397(1-2):69-73. Epub 2006 Jan 10. In rotenone-inhibited HepG2 cells (i.e., already under oxidative stress) MitoQ (10) sharply decreased rotenone-induced J (m), but not together with the Complex II inhibitor thenoyltrifluoroacetone. |
4(0,0,0,4) | Details |
19366681 | Hoffman DL, Brookes PS: From such data, the apparent Km for O2 of putative ROS-generating sites within mitochondria was estimated as follows: 0.2, 0.9, 2.0, and 5.0 microM O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of beta-oxidation, respectively. |
sensitivity of mitochondrial reactive species generation depends on metabolic conditions. Biochem Pharmacol. 1995 May 11;49(9):1303-11.2(0,0,0,2) | Details |
8898917 | Rigoulet M, Devin A, Averet N, Vandais B, Guerin B: Mechanisms of inhibition and uncoupling of respiration in isolated rat liver mitochondria by the general anesthetic 2,6-diisopropylphenol. Biochim Biophys Acta. 1997 Jan 16;1318(1-2):246-54. Diisopropylphenol strongly inhibits state-3 and uncoupled respiratory rates, when and are the substrates, as a direct consequence of the limitation of electron transfer at the level of complex I. |
2(0,0,0,2) | Details |
10371218 | Braidot E, Petrussa E, Vianello A, Macri F: mitochondria oxidizing complex I or complex II substrates. Nucl Med Biol. 1995 Jan;22(1):65-9. The -dependent H2O2 formation was abolished by but unaffected by rotenone. |
peroxide generation by higher plant 2(0,0,0,2) | Details |
15084427 | Alam M, Mayerhofer A, Schmidt WJ: The neurobehavioral changes induced by bilateral rotenone lesion in medial forebrain bundle of rats are reversed by 131-40. Rotenone (an inhibitor of mitochondrial complex I) has been proposed as a model of Parkinson's disease (PD) as it induces nigrostriatal degeneration associated with alpha-synuclein inclusions. |
1(0,0,0,1) | Details |
10917647 | Ohnishi T, Magnitsky S, Toulokhonova L, Yano T, Yagi T, Burbaev DS, Vinogradov AD, Sled VD: EPR studies of the possible binding sites of the cluster N2, semiquinones, and specific inhibitors of the NADH:quinone oxidoreductase (complex I). Brain Res. 2001 May 4;900(1):72-9. |
1(0,0,0,1) | Details |
19245829 | Tahara EB, Navarete FD, Kowaltowski AJ: Tissue-, substrate-, and site-specific characteristics of mitochondrial reactive species generation. Biochem J. 1996 Jan 1;313 ( Pt 1):327-34. The locations and properties of reactive species formation were determined using oxidative phosphorylation and the respiratory chain modulators oligomycin, rotenone, myxothiazol, and antimycin A and the uncoupler CCCP. Our findings support an important participation of flavoenzymes and complex III and a substantial role for reverse electron transport to complex I as reactive species sources. |
1(0,0,0,1) | Details |
19562601 | Henderson JR, Swalwell H, Boulton S, Manning P, McNeil CJ, Birch-Machin MA: Direct, real-time monitoring of mitochondria. Diabetologia. 2005 Mar;48(3):586-94. Epub 2005 Feb 24. The non-invasive sensor system described allowed a comparison of [image omitted] production following specific inhibition of complex I and complex III of the mETC to be made directly and in real-time. |
generation in isolated 1(0,0,0,1) | Details |
12736522 | Xu ZF, Wei XY, Xie HH, Yang RZ: Inhibitory activities of three annonaceous acetogenins on oxidase of chicken liver mitochondria. J Neurochem. 1999 Jul;73(1):220-8. Annonaceous acetogenins (ACG) are natural products found in the plant family Annonaceae and which strongly inhibited mitochondrial complex I. The inhibition of oxidase of chicken liver mitochondria by three different structural ACG was studied here, and ACG was shown to have potent inhibitory activities similar to rotenone for oxidase. |
1(0,0,0,1) | Details |
18298370 | Isaev NK, Stelmashook EV, Dirnagl U, Plotnikov EY, Kuvshinova EA, Zorov DB: Mitochondrial free radical production induced by deprivation in cerebellar granule neurons. Biochemistry. 2008 Feb;73(2):149-55. Inhibitors of mitochondrial electron transport, i.e. rotenone (complex I), antimycin A (complex III), or azide (complex IV), an inhibitor of mitochondrial ATP synthase--oligomycin, an uncoupler of oxidative phosphorylation--CCCP, a chelator of intracellular Ca2+--BAPTA, an inhibitor of electrogenic mitochondrial Ca2+ transport--ruthenium red, as well as significantly decreased neuronal ROS production induced by GD. |
81(1,1,1,1) | Details |
15941011 | Terzi A, Iraz M, Sahin S, Ilhan A, Idiz N, Fadillioglu E: Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue. Toxicol Ind Health. 2004 Sep;20(6-10):141-7. Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. |
81(1,1,1,1) | Details |
15557194 | Woo CH, Lim JH, Kim JH: Lipopolysaccharide induces matrix metalloproteinase-9 expression via a mitochondrial reactive species-p38 kinase-activator protein-1 pathway in Raw 264.7 cells. Mol Biol Rep. 2008 Sep;35(3):397-403. Epub 2007 May 26. LPS-induced MMP-9 expression and p38 kinase phosphorylation were also inhibited by rotenone, a specific inhibitor of mitochondrial complex I, supporting the role of mitochondrial ROS in LPS signaling to MMP-9. |
81(1,1,1,1) | Details |
19707849 | Moldzio R, Radad K, Krewenka C, Kranner B, Duvigneau JC, Wang Y, Rausch WD: Effects of rotenone-injured murine brain cultures. FEBS Lett. 2005 Jul 18;579(18):4005-11. Rotenone is a potent inhibitor of complex I of the respiratory chain, which in vitro causes pathological and neurochemical characteristics of diseases in which mitochondrial impairment is involved, e.g., Parkinson's disease. |
on 81(1,1,1,1) | Details |
16687518 | Keeney PM, Xie J, Capaldi RA, Bennett JP Jr: Parkinson's disease brain mitochondrial complex I has oxidatively damaged subunits and is functionally impaired and misassembled. Free Radic Res. 2009 Sep;43(9):796-802. Epub 2009 Jun 25. This complex I auto-oxidation may derive from abnormalities in mitochondrial or nuclear encoded subunits, complex I assembly factors, rotenone-like complex I toxins, or some combination. |
36(0,1,1,6) | Details |
19096098 | Fato R, Bergamini C, Leoni S, Lenaz G: Mitochondrial production of reactive species: role of complex I and analogues. Neurochem Res. 2005 Sep;30(9):1191-200. The presence of specific inhibitors modulates reactive species production in Complex I: inhibitors such as rotenone induce a strong ROS increase, while inhibitors such as stigmatellin prevent it. |
36(0,1,1,6) | Details |
10097178 | Schuler F, Yano T, Di Bernardo S, Yagi T, Yankovskaya V, Singer TP, Casida JE: quinone oxidoreductase: PSST subunit couples electron transfer from iron- cluster N2 to Brain Res. 2001 Nov 16;919(1):106-14. Complex I and NDH-1 are very sensitive to inhibition by a variety of structurally diverse toxicants, including rotenone, piericidin A, bullatacin, and pyridaben. |
-33(0,1,1,3) | Details |
16120400 | Cameron JM, Levandovskiy V, MacKay N, Robinson BH: Respiratory chain analysis of skin fibroblasts in mitochondrial disease. . J Clin Invest. 1987 Jul;80(1):71-7. NADH:ubiquinone dehydrogenase (complex I) deficiency can be diagnosed from cultured skin fibroblasts using a number of methods, the most commonly used is a linked assay of rotenone-sensitive complex I + III activity (NADH:cytochrome c reductase). |
33(0,1,1,3) | Details |
1753716 | Lamperth L, Dalakas MC, Dagani F, Anderson J, Ferrari R: Abnormal skeletal and cardiac muscle mitochondria induced by zidovudine (AZT) in human muscle in vitro and in an animal model. Curr Med Chem. 2003 Dec;10(23):2507-16. Study of the mitochondrial functions assessed by evaluating stimulated consumption rate, enzymatic activities of electron transport chain and coupling state of oxidative phosphorylation (respiratory control ratio) revealed a decrease in rotenone-sensitive cytochrome C reductase (complex I + III) and an uncoupling effect demonstrated by decreased respiratory control ratio. |
32(0,1,1,2) | Details |
16699582 | Chen Y, Suzuki I: Electron transport pathways for the oxidation of endogenous substrate (s) in Acidithiobacillus ferrooxidans. Lab Invest. 1991 Dec;65(6):742-51. The oxidation was inhibited by complex I inhibitors (rotenone, amytal, and piericidin A) only partially, but piericidin A inhibited the oxidation with Fe3+ nearly completely. |
32(0,1,1,2) | Details |
16410252 | Moreira PI, Custodio J, Moreno A, Oliveira CR, Santos MS: Tamoxifen and interact with the site of complex I leading to mitochondrial failure. Oncogene. 2000 Aug 10;19(34):3840-8. Furthermore, using two respiratory chain inhibitors, rotenone and diphenyliodonium we identified the site of complex I as the target of tamoxifen and/or action (s). |
32(0,1,1,2) | Details |
15515888 | Fujita K, Tani K, Usuki Y, Tanaka T, Taniguchi M: Growth inhibition dependent on reactive derivative of the antifungal antibiotic UK-2A, in Saccharomyces cerevisiae. J Neurochem. 1992 Aug;59(2):746-9. The addition of both a complex I inhibitor rotenone and a complex II inhibitor thenoyltrifluoroacetone reduced ROS generation induced by C9-UK-2A in the whole cells and the isolated mitochondria. |
species generated by C9-UK-2A, a 31(0,1,1,1) | Details |
20349346 | Fujita Y, Hosokawa M, Fujimoto S, Mukai E, Abudukadier A, Obara A, Ogura M, Nakamura Y, Toyoda K, Nagashima K, Seino Y, Inagaki N: suppresses hepatic gluconeogenesis and lowers fasting blood levels through reactive species in mice. Diabetologia. 2010 Mar 29. Since is a mild mitochondrial complex I inhibitor, we compared its effects on suppression of gluconeogenesis, AMPK activation and generation of the RNS (ONOO (-)) with those of rotenone, a representative complex I inhibitor. |
31(0,1,1,1) | Details |
9305406 | Klohn PC, Neumann HG: Impairment of respiration and oxidative phosphorylation by redox cyclers 2-nitrosofluorene and NOF reacts with the NADH:ubiquinone oxidoreductase (complex I) and consumes in a rotenone-insensitive manner. |
Biochim Biophys Acta. 1999 Jan 5;1409(3):143-53.31(0,1,1,1) | Details |
15000895 | Zhang HX, Du GH, Zhang JT: Assay of mitochondrial functions by resazurin in vitro. PLoS One. 2009 Sep 18;4(9):e7100. However, the typical complex I inhibitor, rotenone enhanced the fluorescence intensity without mitochondria. |
31(0,1,1,1) | Details |
8892026 | Pitkanen S, Feigenbaum A, Laframboise R, Robinson BH: NADH-coenzyme Q reductase (complex I) deficiency: heterogeneity in phenotype and biochemical findings. J Biol Chem. 2003 Mar 7;278(10):8516-25. Epub 2002 Dec 20. Each patient also had decreased rotenone-sensitive -cytochrome c reductase (complexes I and III) with normal cytochrome c reductase (complexes II and III) and cytochrome oxidase (complex IV) activity in cultured skin fibroblasts, indicating a deficient NADH-coenzyme Q reductase (complex I) activity. |
31(0,1,1,1) | Details |
15268949 | Chen Y, Suzuki I: Effect of uncouplers on endogenous respiration and ferrous iron oxidation in a chemolithoautotrophic bacterium Acidithiobacillus (Thiobacillus) ferrooxidans. J Bioenerg Biomembr. 2008 Aug;40(4):297-305. Epub 2008 Sep 17. Complex I inhibitors, atabrine, rotenone and amytal inhibited Fe2+ oxidation, more strongly in the presence of 0.1 mM DNP. |
31(0,1,1,1) | Details |
19196431 | Guglielmotto M, Aragno M, Autelli R, Giliberto L, Novo E, Colombatto S, Danni O, Parola M, Smith MA, Perry G, Tamagno E, Tabaton M: The up-regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1alpha. Mol Ther. 2002 Sep;6(3):336-41. The involvement of reactive species released by mitochondria in the BACE1 up-regulation was confirmed by the complete protection exerted by complex I inhibitors such as rotenone and diphenyl-phenylen iodonium. |
31(0,1,1,1) | Details |
17600838 | Tretter L, Takacs K, Kover K, Adam-Vizi V: Stimulation of H (2) O (2) generation by brain mitochondria respiring on IUBMB Life. 2001 Apr;51(4):263-8. In those mitochondria where RET was eliminated by the Complex I inhibitor rotenone (2 microM) or due to depolarization by ADP (1 mM), the rate of H (2) O (2) formation was smaller and the stimulation of H (2) O (2) generation by Ca (2+) was prevented partly, but the stimulatory effect of Ca (2+) was still significant. |
in 31(0,1,1,1) | Details |
14962977 | Ruan Q, Lesort M, MacDonald ME, Johnson GV: Striatal cells from mutant huntingtin knock-in mice are selectively vulnerable to mitochondrial complex II inhibitor-induced cell death through a non-apoptotic pathway. Neurochem Int. 2007 Jan;50(1):189-95. Epub 2006 Sep 8. In contrast, the extent of cell death induced by rotenone, a complex I inhibitor, was similar in both cell lines. |
31(0,1,1,1) | Details |
7873673 | Maklashina EO, Vinogradov AD: [Participation of the complex I from an inactive to active state]. J Cell Biochem. 2004 Feb 1;91(2):384-97. The rotenone-sensitive oxidase was reconstituted from bovine heart Complex I and Escherichia coli -oxidase. |
acceptor in the transition of 11(0,0,1,6) | Details |
10702521 | Brooks H, Krahenbuhl S: Development of a new assay for complex I of the respiratory chain. J Biol Chem. 2009 Jun 12;284(24):16236-45. Epub 2009 Apr 14. Sensitivity to rotenone was used as a measure of complex I specific activity. |
11(0,0,1,6) | Details |
12627969 | Peng G, Fritzsch G, Zickermann V, Schagger H, Mentele R, Lottspeich F, Bostina M, Radermacher M, Huber R, Stetter KO, Michel H: Isolation, characterization and electron microscopic single particle analysis of the NADH:ubiquinone oxidoreductase (complex I) from the hyperthermophilic eubacterium Aquifex aeolicus. J Neurochem. 1996 Mar;66(3):1174-81. The A. aeolicus complex I is completely sensitive to rotenone and 2-n-decyl-quinazoline-4-yl-amine. |
11(0,0,1,6) | Details |
15763667 | Mariano AB, Valente C, Cadena SM, Rocha ME, de Oliveira MB, Carnieri EG: Sensitivities of the alternative respiratory components of potato tuber mitochondria to thiol reagents and Ca2+. BMC Neurosci. 2008 Jan 8;9:4. Another feature of plant mitochondria is that besides complex I (EC 1.6.5.3) they possess alternative NAD (P) H-dehydrogenases insensitive to rotenone. |
6(0,0,1,1) | Details |
18291703 | Dlaskova A, Hlavata L, Jezek P: Oxidative stress caused by blocking of mitochondrial complex I H (+) pumping as a link in aging/disease vicious cycle. Am J Physiol Cell Physiol. 2008 May;294(5):C1124-32. Epub 2008 Mar 19. Rotenone caused a 5-fold J (m) increase (AC (50) 2 microM), which was attenuated by uncoupling, membrane potential (DeltaPsi (m)), and DeltapH-collapse, since addition of FCCP (IC (50) 55 nM), valinomycin, and nigericin prevented this increase. |
6(0,0,0,6) | Details |
1904460 | Harbord MG, Hwang PA, Robinson BH, Becker LE, Hunjan A, Murphy EG: Infant-onset progressive myoclonus epilepsy. . Biochem Pharmacol. 1996 Jun 14;51(11):1503-11. Respiratory-chain enzyme studies were performed on five samples and in three children (all of whom had a history of elevated lactate in serum or cerebrospinal fluid), there were low levels of rotenone-sensitive cytochrome c reductase characteristic of a defect in the complex I part of the respiratory-chain pathway. |
6(0,0,1,1) | Details |
9733090 | Barja G, Herrero A: Localization at complex I and mechanism of the higher free radical production of brain nonsynaptic mitochondria in the short-lived rat than in the longevous pigeon. J Biol Chem. 2003 Sep 26;278(39):37948-56. Epub 2003 Jul 3. Rotenone, antimycin A, and myxothiazol maximally stimulated free radical production with / but not with |
3(0,0,0,3) | Details |
215123 | Heron C, Ragan CI, Trumpower BL: The interaction between mitochondrial NADH-ubiquinone oxidoreductase and -cytochrome c oxidoreductase. Biochem J. 1978 Sep 15;174(3):791-800. Such behaviour can be restored to the interaction between purified Complex I and Complex III by addition of phospholipid and to a concentrated mixture of the Complexes before dilution. 3. |
3(0,0,0,3) | Details |
8535408 | Taniuchi H, Fujibayashi Y, Okazawa H, Yonekura Y, Konishi J, Yokoyama A: Cu-complex with selective -dependent reduction by complex I in brain mitochondria: a potential radiopharmaceutical for mitochondria-functional imaging with positron emission tomography (PET). Biol Pharm Bull. 1995 Aug;18(8):1126-9. Rotenone and antimycin A activated the reduction of Cu-PTSM in the brain mitochondria by 1.6- and 1.4-fold, respectively, compared with untreated controls, while thenoyltrifluoroacetone (TTFA) had no effect on the reduction. |
-bis (N4-methylthiosemicarbazone) (Cu-PTSM), a metal 2(0,0,0,2) | Details |
15377162 | Meyer MJ, Mosely DE, Amarnath V, Picklo MJ Sr: Metabolism of 4- -trans-2-nonenal by central nervous system mitochondria is dependent on age and NAD+ availability. Biochemistry. 2006 Aug 15;45(32):9778-87. Complex I inhibition with respiratory substrates further blocked HNE detoxification. Rotenone (100 nM) inhibited respiration by 15% whereas HNEAcid formation was decreased to 72% of control levels. |
2(0,0,0,2) | Details |
15465329 | Andreani A, Granaiola M, Leoni A, Locatelli A, Morigi R, Rambaldi M, Recanatini M, Lenaz G, Fato R, Bergamini C: Effects of new complex I -ubiquinone reductase) and on mitochondrial permeability transition pore. Eur J Biochem. 1983 Dec 1;137(1-2):113-8. Moreover the low rotenone sensitivity for almost all of these compounds suggests that they are only partially able to interact with the physiological -reduction site. |
-imidazo [2,1-b] thiazoles on mitochondrial 2(0,0,0,2) | Details |
8216312 | Debise R, Touraille S, Durand R, Alziari S: Biochemical consequences of a large deletion in the mitochondrial genome of a Drosophila subobscura strain. Free Radic Biol Med. 1994 Aug;17(2):117-26. Spectrophotometric determination of respiratory complex activities shows that: complex I (5 genes implicated in deletion) presents maximal activity reduced by 40%, whereas that of complex III (concerned by cytochrome b) is lowered by 30%. |
2(0,0,0,2) | Details |
12517982 | Blackstone NW: Redox signaling in the growth and development of colonial hydroids. Clin Chem. 2007 Apr;53(4):729-34. Epub 2007 Mar 1. uptake of colonies was measured to determine comparable physiological doses of antimycin A (1) (an inhibitor of complex III), rotenone (an inhibitor of complex I) and carbonyl m-chlorophenylhydrazone (CCCP; an uncoupler of oxidative phosphorylation). uptake of colonies was measured to determine comparable physiological doses of antimycin A (1) (an inhibitor of complex III), rotenone (an inhibitor of complex I) and carbonyl m-chlorophenylhydrazone (CCCP; an uncoupler of oxidative phosphorylation). |
2(0,0,0,2) | Details |
8603732 | Merlo Pich M, Bovina C, Formiggini G, Cometti GG, Ghelli A, Parenti Castelli G, Genova ML, Marchetti M, Semeraro S, Lenaz G: Inhibitor sensitivity of respiratory complex I in human platelets: a possible biomarker of ageing. Behav Brain Res. 2004 May 5;151(1-2):117-24. The enzyme activities were not significantly changed in the two groups, but a decrease of sensitivity to the specific inhibitor, rotenone, occurred in a substantial number of aged individuals. |
1(0,0,0,1) | Details |
17533645 | Annunen-Rasila J, Ohlmeier S, Tuokko H, Veijola J, Majamaa K: Proteome and cytoskeleton responses in osteosarcoma cells with reduced OXPHOS activity. J Toxicol Environ Health A. 2006 Sep;69(18):1681-97. We describe here the cellular responses to OXPHOS deficiency in osteosarcoma cells upon complex I (CI) and complex IV (CIV) inhibition, and upon the lack of mitochondrial DNA (rho0 cells). |
1(0,0,0,1) | Details |
17050618 | Sridharan V, Guichard J, Bailey RM, Kasiganesan H, Beeson C, Wright GL: The prolyl hydroxylase mitochondrial membrane potential during metabolic inhibition. Biochem Int. 1990 Oct;22(2):303-9. Thus, continued complex I activity was implicated in the maintenance of DeltaPsi (mito) in PHI-treated myocytes, whereas a role for the "reverse mode" operation of the F (1) F (0)-ATP synthase was ruled out. Inclusion of rotenone, but not oligomycin, with and 2-DG was found to collapse DeltaPsi (mito) in PHI-pretreated myocytes. |
-sensing pathway is cytoprotective and allows maintenance of 1(0,0,0,1) | Details |
6536673 | Landi L, Pasquali P, Cabrini L, Sechi AM, Lenaz G: On the mechanism of inhibition of oxidase by -3. Am J Physiol Cell Physiol. 2007 Feb;292(2):C719-28. Epub 2006 Oct 18. The combined effects of rotenone and -3 on the kinetics of NADH dehydrogenase and oxidase have been investigated. The inhibition of oxidase by -3 is the result of at least two combined effects: the competition of the less active -3 with endogenous in the acceptor site of the dehydrogenase, and a nonspecific action on the structure of complex I. |
1(0,0,0,1) | Details |
12080052 | Damdimopoulos AE, Miranda-Vizuete A, Pelto-Huikko M, Gustafsson JA, Spyrou G: Human mitochondrial thioredoxin. J Bioenerg Biomembr. 1984 Apr;16(2):153-66. In addition, HEK-Trx2 are more sensitive toward rotenone, an inhibitor of complex I of the respiratory chain. In addition, HEK-Trx2 are more sensitive toward rotenone, an inhibitor of complex I of the respiratory chain. |
1(0,0,0,1) | Details |
11527152 | Monti E, Supino R, Colleoni M, Costa B, Ravizza R, Gariboldi MB: function and induces apoptosis in HL60 cells. J Neurosci. 2006 May 10;26(19):5256-64. In addition, TEMPOL was found to specifically target complex I of the respiratory chain, with minor effects on complexes II and IV, suggesting that mitochondrial effects might play a role in TEMPOL-induced oxidative stress and apoptosis, and that TEMPOL might sensitize tumor cells to the pro-apoptotic effects of cytotoxic agents. |
TEMPOL impairs mitochondrial 1(0,0,0,1) | Details |
10366439 | Leist M, Single B, Naumann H, Fava E, Simon B, Kuhnle S, Nicotera P: Inhibition of mitochondrial ATP generation by switches apoptosis to necrosis. FEMS Immunol Med Microbiol. 1999 Jun;24(2):169-74. In contrast, depleting intracellular ATP with rotenone, an inhibitor of mitochondrial complex I mimicked the effect of NO. In contrast, depleting intracellular ATP with rotenone, an inhibitor of mitochondrial complex I mimicked the effect of NO. |
1(0,0,0,1) | Details |
8663005 | Rustin P, Parfait B, Chretien D, Bourgeron T, Djouadi F, Bastin J, Rotig A, Munnich A: Fluxes of membranes in human cultured cells. Arch Biochem Biophys. 2002 Sep 15;405(2):252-64. They also point to the possible confusion between a loss of mitochondrial NAD and a defect of respiratory chain complex I in the context of screening procedures for respiratory chain disorder in human. |
dinucleotides through mitochondrial 1(0,0,0,1) | Details |
12846980 | Fiskum G, Starkov A, Polster BM, Chinopoulos C: Mitochondrial mechanisms of neural cell death and neuroprotective interventions in Parkinson's disease. Mol Pharmacol. 2000 Aug;58(2):271-8. Neurotoxins that induce parkinsonian neuropathology, such as MPP (+) and rotenone, stimulate production at complex I of the electron transport chain and also stimulate free radical production at proximal redox sites including mitochondrial matrix dehydrogenases. |
81(1,1,1,1) | Details |
16659084 | Tomlinson PF, Moreland DE: Mitochondria. . Plant Physiol. 1975 Feb;55(2):365-369. Essentially complete inhibition was obtained with inhibitors of complex I (rotenone, amytal, and thenoyltrifluoroacetone) and complex II (thenoyltrifluoroacetone). |
-resistant Respiration of Sweet Potato 81(1,1,1,1) | Details |
17210467 | VanBrocklin HF, Hanrahan SM, Enas JD, Nandanan E, O'Neil JP: Mitochondrial avid radioprobes. J Neurochem. 1998 Dec;71(6):2549-57. Two tracers, 7'-Z-iodorotenol and 7'-Z-iodorotenone, analogs of rotenone a natural product that inhibits Complex I of the mitochondrial electron transport chain, have been labeled with -125 in 45-85% yield in a single step from the corresponding tributylstannyl precursor. |
81(1,1,1,1) | Details |
19744517 | Hosamani R, Muralidhara: Neuroprotective efficacy of Bacopa monnieri against rotenone induced oxidative stress and neurotoxicity in Drosophila melanogaster. Synapse. 2003 Dec 1;50(3):240-50. Environmental toxins like rotenone, a specific inhibitor of complex I is employed to increase oxidative stress mediated neuropathology and sporadic Parkinson's disease. |
81(1,1,1,1) | Details |
19041852 | Gieseler A, Schultze AT, Kupsch K, Haroon MF, Wolf G, Siemen D, Kreutzmann P: Inhibitory modulation of the mitochondrial permeability transition by minocycline. FEBS Lett. 2005 Dec 19;579(30):6716-20. Epub 2005 Nov 21. Treatment of neuron-enriched cortical cultures with rotenone, a high affinity inhibitor of the mitochondrial complex I, resulted in a deregulation of the intracellular Ca2+-dynamics, as recorded by live cell imaging. |
81(1,1,1,1) | Details |
19174508 | Nguyen KT, Garcia-Chacon LE, Barrett JN, Barrett EF, David G: The Psi (m) depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals. Brain Res. 1998 Oct 26;809(1):12-7. Stimulation-induced Psi (m) depolarization and elevation of cytosolic [Ca (2+)] both increased when complex I of the ETC was partially inhibited by low concentrations of rotenone (25-50 nmol/l). |
81(1,1,1,1) | Details |
10433118 | Combettes B, Grienenberger JM: Analysis of wheat mitochondrial complex I purified by a one-step immunoaffinity chromatography. Neurochem Int. 2005 Jun;46(7):513-21. The complex retained on the column proved to be a functional complex I, since the preparation showed NADH:duroquinone and NADH:FeK3 (CN) 6 reductase activities which were inhibited by rotenone. |
36(0,1,1,6) | Details |
12535666 | Chretien D, Benit P, Chol M, Lebon S, Rotig A, Munnich A, Rustin P: Assay of mitochondrial respiratory chain complex I in human lymphocytes and cultured skin fibroblasts. J Antibiot. 2004 Aug;57(8):511-7. The procedure strongly reduces contaminating NADH:quinone oxidoreductase activity and permits measuring high rates of rotenone-sensitive complex I activity thanks to effective cell permeabilization. |
35(0,1,1,5) | Details |
16893179 | Murai M, Ichimaru N, Abe M, Nishioka T, Miyoshi H: Mode of inhibitory action of Deltalac-acetogenins, a new class of inhibitors of bovine heart mitochondrial complex I. Biochem Biophys Res Commun. 2003 Jan 31;301(1):222-4. We have revealed that Deltalac-acetogenins, a new class of inhibitors of bovine heart mitochondrial complex I (NADH-ubiquinone oxidoreductase), act differently from ordinary inhibitors such as rotenone and piericidin A [Ichimaru et al. (2005) Biochemistry 44, 816-825]. |
35(0,1,1,5) | Details |
20170624 | Grivennikova VG, Kareyeva AV, Vinogradov AD: What are the sources of production by heart mitochondria?. Eur J Biochem. 1984 Jun 15;141(3):573-7. -supported peroxide production by the rotenone-treated mitochondria devoid of a permeability barrier for H (2) O (2) diffusion by alamethicin treatment are only partially ( approximately 50%) sensitive to the Complex I binding site-specific inhibitor, -OH. |
peroxide 33(0,1,1,3) | Details |
18251845 | Juszczuk IM, Flexas J, Szal B, Dabrowska Z, Ribas-Carbo M, Rychter AM: Effect of mitochondrial genome rearrangement on respiratory activity, photosynthesis, photorespiration and energy status of MSC16 cucumber (Cucumis sativus) mutant. J Neurochem. 2001 Oct;79(2):266-77. Decreased respiratory capacity of complex I in MSC16 mitochondria was indicated by lower respiration rates of intact mitochondria with and by rotenone-inhibited or oxidation in the presence of alamethicin. |
33(0,1,1,3) | Details |
14592516 | Tormo JR, Gallardo T, Peris E, Bermejo A, Cabedo N, Estornell E, Zafra-Polo MC, Cortes D: Inhibitory effects on mitochondrial complex I of semisynthetic mono-tetrahydrofuran acetogenin derivatives. Brain Res. 2005 Feb 8;1033(2):143-50. Their inhibitory effects on mitochondrial complex I is discussed and compared with that of the classical complex I inhibitor, rotenone. |
32(0,1,1,2) | Details |
12210849 | Tai KK, Truong DD: Activation of -sensitive channels confers protection against rotenone-induced cell death: therapeutic implications for Parkinson's disease. Plant J. 2001 Oct;28(1):73-82. Here we show that transient activation of ATP-sensitive channels, a trigger in ischemic preconditioning signaling, confers protection in PC12 cells and SH-SY5Y cells against effect of rotenone and MPTP, mitochondrial complex I inhibitors that have been implicated in the pathogenesis of Parkinson's disease. |
31(0,1,1,1) | Details |
10438663 | Di Monte DA, Tokar I, Langston JW: Impaired The effect of MPP (+) on clearance: (i) was accompanied by a decrease in cellular ATP; (ii) could be enhanced by withdrawing from the incubation medium or by inhibiting glycolysis with 2-deoxyglucose, and (iii) could be reproduced using the mitochondrial complex I inhibitor rotenone. |
clearance as a consequence of energy failure caused by MPP (+) in astrocytic cultures. Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):4149-53.31(0,1,1,1) | Details |
17520785 | Yi PL, Tsai CH, Lu MK, Liu HJ, Chen YC, Chang FC: Interleukin-1beta mediates sleep alteration in rats with rotenone-induced parkinsonism. Int J Biochem Cell Biol. 2004 Jan;36(1):162-72. DESIGN: We employed a long-term subcutaneous infusion of rotenone, a mitochondrial complex-I inhibitor, to induce a parkinsonism-like model in rats. |
31(0,1,1,1) | Details |
19781600 | Ahn SY, Choi YS, Koo HJ, Jeong JH, Park WH, Kim M, Piao Y, Pak YK: Mitochondrial dysfunction enhances the migration of vascular smooth muscles cells via suppression of Akt phosphorylation. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Dec;26(6):1191-200. Similarly, dideoxycytidine (ddC), the mtDNA replication inhibitor, or rotenone, OXPHOS complex I inhibitor, inhibited the insulin-mediated pAkt while increased pAMPK regardless of insulin. |
31(0,1,1,1) | Details |
12065751 | Waldmeier PC, Feldtrauer JJ, Qian T, Lemasters JJ: Inhibition of the mitochondrial permeability transition by the nonimmunosuppressive cyclosporin derivative NIM811. BMC Plant Biol. 2004 May 12;4:8. Using two newly developed microtiter plate assays, one measuring mitochondrial swelling from absorbance and the other measuring mitochondrial membrane potential from changes in safranin fluorescence, we show that NIM811 blocks the MPT induced by and inorganic alone or in combination with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, the complex I inhibitor rotenone, and the prooxidant t-butylhydroperoxide. |
31(0,1,1,1) | Details |
12807439 | Jensen PJ, Alter BJ, O'Malley KL: Alpha-synuclein protects naive but not dbcAMP-treated dopaminergic cell types from 1-methyl-4-phenylpyridinium toxicity. Mol Cancer. 2004 Jul 12;3:19. Similarly, alpha-synuclein protected cells from the complex I inhibitor rotenone and 3-nitroproprionic acid, a complex II inhibitor. |
31(0,1,1,1) | Details |
1332758 | Finel M, Skehel JM, Albracht SP, Fearnley IM, Walker JE: Resolution of NADH:ubiquinone oxidoreductase from bovine heart mitochondria into two subcomplexes, one of which contains the redox centers of the enzyme. J Bioenerg Biomembr. 2009 Aug;41(4):379-85. Epub 2009 Oct 10. The line shapes of the EPR spectra of the Fe-S clusters are slightly broadened relative to spectra measured on complex I purified by conventional means, and the quinone reductase activity is insensitive to rotenone. |
11(0,0,1,6) | Details |
12079358 | Cardol P, Matagne RF, Remacle C: Impact of mutations affecting ND mitochondria-encoded subunits on the activity and assembly of complex I in Chlamydomonas. Neurochem Int. 2006 Jul;49(1):28-40. Epub 2006 Feb 21. The mitochondrial rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) comprises more than 35 subunits, the majority of which are encoded by the nucleus. |
11(0,0,1,6) | Details |
11229440 | Goossens V, Stange G, Moens K, Pipeleers D, Grooten J: Regulation of tumor necrosis factor-induced, mitochondria- and reactive species-dependent cell death by the electron flux through the electron transport chain complex I. Neuroscience. 2003;121(2):287-96. |
6(0,0,0,6) | Details |
19097788 | Dong CK, Patel V, Yang JC, Dvorin JD, Duraisingh MT, Clardy J, Wirth DF: Type II NADH dehydrogenase of the respiratory chain of Plasmodium falciparum and its inhibitors. J Biol Chem. 2004 Apr 23;279(17):17197-204. Epub 2004 Feb 11. Plasmodium falciparum NDH2 (pfNDH2) is a non- pumping, rotenone-insensitive alternative enzyme to the multi-subunit NADH:ubiquinone oxidoreductases (Complex I) of many other eukaryotes. |
6(0,0,1,1) | Details |
15047621 | Brunmair B, Staniek K, Gras F, Scharf N, Althaym A, Clara R, Roden M, Gnaiger E, Nohl H, Waldhausl W, Furnsinn C: Thiazolidinediones, like inhibit respiratory complex I: a common mechanism contributing to their antidiabetic actions?. Biochem Pharmacol. 2009 Mar 1;77(5):888-96. Epub 2008 Nov 12. |
6(0,0,0,6) | Details |
9375690 | Davey GP, Canevari L, Clark JB: Threshold effects in synaptosomal and nonsynaptic mitochondria from hippocampal CA1 and paramedian neocortex brain regions. J Neurochem. 1997 Dec;69(6):2564-70. In addition, when complex I and IV activities were titrated with specific inhibitors, thresholds in ATP synthesis and respiration became apparent. |
3(0,0,0,3) | Details |
215122 | Ragan CI, Heron C: The interaction between mitochondrial NADH-ubiquinone oxidoreductase and -cytochrome c oxidoreductase. Circ Res. 2004 Mar 5;94(4):478-86. Epub 2003 Dec 29. The NADH-ubiquinone oxidoreductase complex (Complex I) and the -cytochrome c oxidoreductase complex (Complex III) combine in a 1:1 molar ratio to give -cytochrome c oxidoreductase (Complex I-Complex III). 2. Experiments on the inhibition of the -cytochrome c oxidoreductase activity of mixtures of Complexes I and III by rotenone and antimycin indicate that electron transfer between a unit of Complex I-Complex III and extra molecules of Complexes I or III does not contribute to the overall rate of cytochrome c reduction. 3. |
3(0,0,0,3) | Details |
10797558 | Lamensdorf I, Eisenhofer G, Harvey-White J, Hayakawa Y, Kirk K, Kopin IJ: Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4-dihydroxyphenylacetaldehyde. Arch Biochem Biophys. 1995 Jan 10;316(1):70-6. Using inhibitors of mitochondrial complexes I, II, III and IV we found that inhibition of complex I and III increased levels of DOPAL and DOPET. |
3(0,0,0,3) | Details |
9230920 | Zharova TV, Vinogradov AD: A competitive inhibition of the mitochondrial NADH-ubiquinone oxidoreductase (complex I) by ADP- Neurotoxicol Teratol. 2004 Nov-Dec;26(6):857-64. Ki for inhibition of the rotenone-sensitive oxidase in SMP by ADPR does not depend on delta mu H+. |
2(0,0,0,2) | Details |
15151993 | Gauthier BR, Brun T, Sarret EJ, Ishihara H, Schaad O, Descombes P, Wollheim CB: Oligonucleotide microarray analysis reveals PDX1 as an essential regulator of mitochondrial metabolism in rat islets. Eur J Biochem. 2001 May;268(10):3075-82. In parallel there was a 50% reduction in mRNA levels for the mitochondrially encoded nd1 gene, a subunit of the NADH dehydrogenase comprising complex I of the mitochondrial respiratory chain. Rotenone, an inhibitor of complex I, mimicked this effect. |
2(0,0,0,2) | Details |
8377005 | Krueger MJ, Sablin SO, Ramsay R, Singer TP: Reactivation of NADH dehydrogenase (complex I) inhibited by 1-methyl-4-(4'-alkylphenyl) pyridinium analogues: a clue to the nature of the inhibition site. Exp Mol Pathol. 2005 Jun;78(3):228-32. Epub 2005 Feb 17. MPP+ and its analogues have been shown to block electron transport at or near the same site as two powerful inhibitors of mitochondrial respiration, rotenone and piericidin A. |
2(0,0,0,2) | Details |
15958286 | del Arenal IP, Rubio ME, Ramirez J, Rendon JL, Escamilla JE: complex I with O2. Ukr Biokhim Zh. 2004 Jan-Feb;76(1):56-64. Mitochondrial respiration with as substrate was partially inhibited by rotenone, and antimycin in decreasing order of effectiveness. |
-resistant respiration in Taenia crassiceps metacestode (cysticerci) is explained by the H2O2-producing side-reaction of respiratory 2(0,0,0,2) | Details |
19495971 | Ullrich C, Humpel C: Rotenone Induces Cell Death of Cholinergic Neurons in an Organotypic Co-Culture Brain Slice Model. Am J Physiol Lung Cell Mol Physiol. 2007 Sep;293(3):L809-19. Epub 2007 Jun 29. In summary, inhibition of complex I of the electron transport chain may play a role in neurodegeneration of cholinergic neurons. |
1(0,0,0,1) | Details |
1763894 | Larsson NG, Andersen O, Holme E, Oldfors A, Wahlstrom J: Leber's hereditary optic neuropathy and complex I deficiency in muscle. . J Cell Sci. 2007 Mar 1;120(Pt 5):838-48. Epub 2007 Feb 13. This study showed that there is decreased activity of complex I of the respiratory chain in muscle and that cerebral striatal lesions occur in Leber's hereditary optic neuropathy with the NADH-dehydrogenase 4 gene point mutation. There was no decrease in complex I activity measured as ferricyanide reductase or rotenone-sensitive cytochrome c reductase activities. |
1(0,0,0,1) | Details |
17954696 | Matsumoto J, Sakamoto K, Shinjyo N, Kido Y, Yamamoto N, Yagi K, Miyoshi H, Nonaka N, Katakura K, Kita K, Oku Y: Anaerobic target for the chemotherapy of alveolar echinococcosis. Physiol Plant. 2001 Apr;111(4):448-456. Furthermore, in vitro treatment assays using respiratory chain inhibitors against the -quinone reductase activity of mitochondrial complex I demonstrated that they had a potent ability to kill protoscoleces. |
- reductase system is predominant in the respiratory chain of Echinococcus multilocularis, providing a novel 1(0,0,0,1) | Details |
17877636 | Ma TC, Mihm MJ, Bauer JA, Hoyt KR: Bioenergetic and oxidative effects of free neurons and increased sensitivity of non-dopaminergic neurons to oxidation. Nucl Med Biol. 2007 Jan;34(1):109-16. Epub 2006 Nov 28. Free 3NT alone directly inhibited mitochondrial complex I, decreased ATP, sensitized neurons to mitochondrial depolarization, and increased production. Subtoxic concentrations of rotenone (instead of free 3NT) caused similar results. |
in culture: selective vulnerability of dopaminergic 1(0,0,0,1) | Details |
10951577 | Chandel NS, Vander Heiden MG, Thompson CB, Schumacker PT: Redox regulation of p53 during hypoxia. . J Bioenerg Biomembr. 2008 Aug;40(4):289-96. Epub 2008 Sep 2. Rotenone, an inhibitor of mitochondrial complex I, and 4,4'-diisothiocyanato-stilbene-2,2'-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia. Rotenone, an inhibitor of mitochondrial complex I, and 4,4'-diisothiocyanato-stilbene-2,2'-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia. |
1(0,0,0,1) | Details |
12473378 | Zhou G, Jiang W, Zhao Y, Ma G, Xin W, Yin J, Zhao B: mediates electron transfer reaction in rat heart mitochondria. Brain Res. 1997 Nov 28;777(1-2):110-8. It was found that STS could stimulate mitochondrial oxidation dose-dependently and partly restore oxidation in the presence of respiratory inhibitor (rotenone or antimycin A or KCN). It was likely that STS could accept electrons from complex I similar to ferricyanide and could be converted to its semiquinone form that could then reduce molecule. |
tanshinone IIA sulfonate 1(0,0,0,1) | Details |
6451185 | Rouslin W, Millard RW: Mitochondrial inner membrane enzyme defects in porcine myocardial ischemia. J Neurosci Res. 2006 Nov 1;84(6):1376-84. After 2 h of occlusion, mitochondria from the ischemic area exhibited a 36 +/- 6% drop in state 3 respiratory activity (QO2) supported by the NAD-linked substrates, plus but only a 5 +/- 3% decrease in QO2 with plus rotenone. The activity of electron transfer complex I - reductase) decreased commensurately by 33 +/- 4% with the decrease in QO2 with NAD-linked substrates. |
1(0,0,0,1) | Details |
508289 | Van Hinsbergh VW, Veerkamp JH, Glatz JF: oxidation by rat skeletal-muscle mitochondria. . Antimicrob Agents Chemother. 2006 May;50(5):1841-51. These observations indicate that the branched-chain 2-oxo acid dehydrogenase complex is situated on the inner side of the mitochondrial inner membrane. 6. Addition of rotenone and simultaneous addition of carbonyl p-trifluoromethoxyphenyl-hydrazone (FCCP) and valinomycin markedly decreased oxidation. 5. |
1(0,0,0,1) | Details |
8945906 | Goda N, Suematsu M, Mukai M, Kiyokawa K, Natori M, Nozawa S, Ishimura Y: Modulation of mitochondrion-mediated oxidative stress by in human placental trophoblastic cells. Oncogene. 1998 Nov 12;17(19):2515-24. This oxidative process was completely blocked by rotenone, a reagent that interferes with electron entry into complex I of the mitochondrial respiratory chain. |
81(1,1,1,1) | Details |
17504811 | Guidarelli A, Cerioni L, Cantoni O: Inhibition of complex III promotes loss of Ca2+ dependence for mitochondrial formation and permeability transition evoked by Brain Res. 2008 Dec 3;1243:167-73. Epub 2008 Sep 30. Here we show that formation of H2O2 and DNA damage are suppressed by inhibition of complex I (by rotenone) or formation (by myxothiazol), as well as by a variety of manipulations preventing either the mobilization of Ca2+ or its mitochondrial accumulation. |
81(1,1,1,1) | Details |
12832841 | Kitamura Y, Inden M, Sanada H, Takata K, Taniguchi T, Shimohama S, Orii H, Mochii M, Agata K, Watanabe K: Inhibitory effects of antiparkinsonian drugs and caspase inhibitors in a parkinsonian flatworm model. Exp Neurol. 2004 Jan;185(1):169-81. It has been known that rotenone and 1-methyl-4-phenylpyridinium ion (MPP (+), a metabolite of MPTP), which inhibit mitochondrial complex I, are useful tools for parkinsonian models in vertebrates such as primates and rodents. |
81(1,1,1,1) | Details |
18437094 | Riess ML, Camara AK, Heinen A, Eells JT, Henry MM, Stowe DF: KATP channel openers have opposite effects on mitochondrial respiration under different energetic conditions. Ukr Biokhim Zh. 2003 Sep-Oct;75(5):69-76. consumption was measured for complex I / or complex II with rotenone) substrates in mitochondria from fresh guinea pig hearts. |
81(1,1,1,1) | Details |
12171069 | Magnitsky S, Toulokhonova L, Yano T, Sled VD, Hagerhall C, Grivennikova VG, Burbaev DS, Vinogradov AD, Ohnishi T: EPR characterization of ubisemiquinones and iron-NADH-ubiquinone oxidoreductase (complex I) in situ. Am J Physiol Renal Physiol. 2004 Apr;286(4):F749-59. Epub 2003 Dec 9. In the current study, special attention was placed on the SQNf, because of its high sensitivities to DeltamicroH+ and to specific complex I inhibitors (rotenone and piericidin A) in a unique manner. |
cluster N2, central components of the energy coupling in the 35(0,1,1,5) | Details |
18781777 | Ichimaru N, Murai M, Kakutani N, Kako J, Ishihara A, Nakagawa Y, Nishioka T, Yagi T, Miyoshi H: Synthesis and characterization of new piperazine-type inhibitors for mitochondrial NADH-ubiquinone oxidoreductase (complex I). Biofactors. 1998;8(3-4):195-204. The mode of action of Deltalac-acetogenins, strong inhibitors of bovine heart mitochondrial complex I, is different from that of traditional inhibitors such as rotenone and piericidin A [Murai, M., et al. (2007) Biochemistry 46 , 6409-6416]. |
35(0,1,1,5) | Details |
12057837 | Zhang X, Jones D, Gonzalez-Lima F: Mouse model of optic neuropathy caused by mitochondrial complex I dysfunction. Free Radic Biol Med. 2009 May 1;46(9):1283-97. Epub 2009 Feb 23. We developed a mouse model of optic neuropathy caused by mitochondrial complex I dysfunction by intravitreal administration of rotenone, a complex I inhibitor, in CBA/J mice. |
33(0,1,1,3) | Details |
18812510 | Choi WS, Kruse SE, Palmiter RD, Xia Z: Mitochondrial complex I inhibition is not required for dopaminergic neuron death induced by rotenone, MPP+, or paraquat. J Pharmacol Exp Ther. 1998 Mar;284(3):1112-21. These data suggest that dopaminergic neuron death induced by treatment with rotenone, MPP (+), or paraquat is independent of complex I inhibition. |
33(0,1,1,3) | Details |
18703762 | Audi SH, Merker MP, Krenz GS, Ahuja T, Roerig DL, Bongard RD: metabolism during passage through the rat pulmonary circulation and the effect of hyperoxia. Brain Res. 1997 Nov 28;777(1-2):202-9. In normoxic lungs, CoQ (1) H (2) efflux rates when CoQ (1) was infused decreased by 58 and 33% in the presence of rotenone (mitochondrial complex I inhibitor) and dicumarol [NAD (P) H-quinone oxidoreductase 1 (NQO1) inhibitor], respectively. |
redox 33(0,1,1,3) | Details |
15505787 | Valentino ML, Barboni P, Ghelli A, Bucchi L, Rengo C, Achilli A, Torroni A, Lugaresi A, Lodi R, Barbiroli B, Dotti M, Federico A, Baruzzi A, Carelli V: The ND1 gene of complex I is a mutational hot spot for Leber's hereditary optic neuropathy. Am J Physiol Renal Physiol. 2007 Sep;293(3):F723-31. Epub 2007 Jun 27. Biochemical investigations in platelets showed partially insensitive complex I to rotenone inhibition. |
32(0,1,1,2) | Details |
15905875 | Ladha JS, Tripathy MK, Mitra D: Mitochondrial complex I activity is impaired during HIV-1-induced T-cell apoptosis. FEBS Lett. 1997 Jul 28;412(2):265-9. Finally, sensitivity to complex I inhibitor Rotenone is reduced in HIV-1-infected T cells indicating an important role for it in the death process. |
32(0,1,1,2) | Details |
19009337 | Wen JJ, Garg NJ: Mitochondrial generation of reactive complex III in the myocardium of Trypanosoma cruzi-infected mice: beneficial effects of an antioxidant. Antioxid Redox Signal. 1999 Spring;1(1):97-104. Inhibition studies with normal cardiac mitochondria showed that rotenone induced ROS generation at the Q (Nf)- site in complex I. |
species is enhanced at the Q (o) site of the 32(0,1,1,2) | Details |
19633536 | Li Y, Rory Goodwin C, Sang Y, Rosen EM, Laterra J, Xia S: Camptothecin and Fas receptor agonists synergistically induce medulloblastoma cell death: ROS-dependent mechanisms. Eur J Cell Biol. 2004 Mar;83(2):51-4. Moreover, the mitochondrial respiratory chain complex I inhibitor rotenone potentiated CH-11-induced apoptosis in DAOY cells. |
31(0,1,1,1) | Details |
15146976 | Bocklinger K, Tomaselli B, Heftberger V, Podhraski V, Bandtlow C, Baier-Bitterlich G: hypoxia. Rev Esp Geriatr Gerontol. 2009 Jul-Aug;44(4):194-9. Epub 2009 Jul 3. Rotenone, a mitochondrial complex I inhibitor, induced a 30.4 +/- 3.6% loss of viable cells and a 35.0 +/- 4.4% loss of neurite formation of cerebellar granule cells, which was partially restored by the addition of nucleosides and |
nucleosides support the neurite outgrowth of primary rat cerebellar granule cells after 31(0,1,1,1) | Details |
7994564 | Chen CL, Sangiah S, Yu CA, Chen H, Berlin KD, Garrison GL, Scherlag BJ, Lazzara R: Effects of novel antiarrhythmic agents, BRB-I-28 and its derivatives, on the heart mitochondrial respiratory chain and sarcoplasmic reticulum Ca (2+)-ATPase. Res Commun Mol Pathol Pharmacol. 1994 Aug;85(2):193-208. The site of inhibition of BRB-I-28 and its derivatives on the respiratory chain was localized between flavoprotein n (FPn) and which is similar to the effect of rotenone and several other antiarrhythmic drugs such as amiodarone, etc. |
0(0,0,0,0) | Details |
18471434 | Lombardi A, Grasso P, Moreno M, de Lange P, Silvestri E, Lanni A, Goglia F: Interrelated influence of superoxides and free fatty acids over mitochondrial uncoupling in skeletal muscle. Eukaryot Cell. 2006 Sep;5(9):1460-7. In the absence of FFAs, no differences in -leak kinetic were detected between -energized mitochondria respiring in the absence or presence of rotenone, despite a large difference in complex I production. |
0(0,0,0,0) | Details |
11989755 | Bottje W, Iqbal M, Tang ZX, Cawthon D, Okimoto R, Wing T, Cooper M: Association of mitochondrial function with feed efficiency within a single genetic line of male broilers. Poult Sci. 2002 Apr;81(4):546-55. Electron leak increased following inhibition of electron transport at Complex I (with rotenone) and Complex III (with antimycin A) in low FE but not in high FE breast mitochondria. |
0(0,0,0,0) | Details |
12376345 | Schroedl C, McClintock DS, Budinger GR, Chandel NS: Hypoxic but not anoxic stabilization of HIF-1alpha requires mitochondrial reactive Primary evidence for this model comes from the observation that cells treated with complex I inhibitors, such as rotenone, or cells that lack mitochondrial DNA (rho (0)-cells) fail to generate reactive species or stabilize HIF-1alpha protein in response to hypoxia. |
species. Mol Cell Biochem. 2008 Jul;314(1-2):45-50. Epub 2008 Apr 15.0(0,0,0,0) | Details |
18224432 | Shiryaeva A, Baidyuk E, Arkadieva A, Okovityy S, Morozov V, Sakuta G: Hepatocyte mitochondrion electron-transport chain alterations in CCl (4) and induced hepatitis in rats and their correction with Biochim Biophys Acta. 2006 May-Jun;1757(5-6):553-61. Epub 2006 Apr 17. The presented data lead to the assumption that the increased consumption by the respiratory chain of pathological mitochondria to be linked mainly with the altered function of complex I. Rotenone resulted in 27% suppression of respiration by pathological hepatocytes whereas 2,4-dinitrophenol produced a 1.4-fold increase of respiration. |
1(0,0,0,1) | Details |
12958040 | Cowan DB, Jones M, Garcia LM, Noria S, del Nido PJ, McGowan FX Jr: Hypoxia and stretch regulate intercellular communication in vascular smooth muscle cells through reactive species formation. J Neurosci Res. 2008 Aug 1;86(10):2339-52. Using a fluorogenic substrate, hypoxic VSMCs showed increased reactive species generation, which could be prevented by the peroxidase mimic ebselen and the mitochondrial complex I inhibitor rotenone but not with the redox-sensitive thiol pyrrolidine dithiocarbamate. |
0(0,0,0,0) | Details |
15694918 | Kotake Y, Taguchi R, Okuda K, Sekiya Y, Tasaki Y, Hirobe M, Ohta S: Neuroprotective effect of 1-methyl-1,2,3,4-tetrahydroisoquinoline on cultured rat mesencephalic neurons in the presence or absence of various neurotoxins. J Biol Chem. 2003 Sep 19;278(38):36027-31. Epub 2003 Jul 2. In this study, we examined the neuroprotective effect of 1MeTIQ against four dopaminergic neurotoxins, 1-methyl-4-phenylpyridinuim ion, rotenone, and l-benzyl-1,2,3,4-tetrahydroisoquinoline, in cultured rat mesencephalic neurons. 1MeTIQ exerted neuroprotective action against all these toxins. |
0(0,0,0,0) | Details |
9396723 | Guidarelli A, Clementi E, Brambilla L, Cantoni O: Mechanism of the antimycin A-mediated enhancement of t-butylhydroperoxide-induced single-strand breakage in DNA. Chem Biol Interact. 2004 Dec 7;150(3):253-70. The hypothesis that these effects are selectively linked to inhibition of the electron transport from cytochrome b to cytochrome c1 is validated by the following observations: (1) two complex III inhibitors, antimycin A and 2-heptyl-4-hydroxyquinoline N-oxide, enhanced the tB-OOH-induced DNA cleavage over the same concentration range as that in which inhibition of consumption was observed; (2) the complex III inhibitor-mediated enhancement of tB-OOH-induced DNA damage was abolished by the complex I inhibitor rotenone or by omission, and (3) the enhancing effects of antimycin A were not observed in respiration-deficient cells. |
0(0,0,0,0) | Details |
17343987 | Alvira D, Tajes M, Verdaguer E, de Arriba SG, Allgaier C, Matute C, Trullas R, Jimenez A, Pallas M, Camins A: Inhibition of cyclin-dependent kinases is neuroprotective in 1-methyl-4-phenylpyridinium-induced apoptosis in neurons. J Bioenerg Biomembr. 2008 Feb;40(1):27-34. Epub 2008 Jan 26. Mitochondrial dysfunction, specifically alteration of the mitochondrial complex I, is the primary target of the parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP+) induced apoptosis in neurons. |
1(0,0,0,1) | Details |
3134033 | Filser M, Werner S: Pethidine analogues, a novel class of potent inhibitors of mitochondrial ubiquinone reductase. J Neurochem. 2005 Feb;92(4):840-9. Dose-response curves revealed that the potency of these compounds is very comparable to that of the standard probe rotenone. The potential advantages of the pethidine derivatives for the investigation of structure - function relationships within complex I of the respiratory chain is discussed. |
1(0,0,0,1) | Details |
17900761 | Larsen TR, Soderling AS, Caidahl K, Roepstorff P, Gramsbergen JB: Nitration of soluble proteins in organotypic culture models of Parkinson's disease. J Neurosci. 2002 Aug 15;22(16):7006-15. Here we quantified protein-bound (3-NT) by a novel gas chromatography/negative chemical ionization tandem mass spectrometry technique and DA and by HPLC in tissues or medium of organotypic, mouse mesencephalon cultures after acute or chronic treatments with the donor 3-morpholino-sydnonimine (SIN-1), the dopaminergic toxin 1-methyl-4-phenylpyridinium (MPP (+)) or the lipophilic complex I inhibitor rotenone. |
0(0,0,0,0) | Details |
17596522 | Zhang A, Jia Z, Guo X, Yang T: epithelial-mesenchymal transition via ROS of mitochondrial origin. Biochim Biophys Acta. 2007 Jul;1767(7):940-7. Epub 2007 Apr 6. Aldo-induced oxidative stress and EMT were both abolished by the mitochondrial respiratory chain complex I inhibitor rotenone, but not the oxidase inhibitor apocynin. |
induces 0(0,0,0,0) | Details |
6317378 | Demant EJ: oxidation in submitochondrial particles protects respiratory chain activity against damage by adriamycin-Fe3+. Neurotoxicology. 2009 Jul;30(4):589-98. Epub 2009 Apr 1. Protection by is strengthened by removal of cytochrome c from the submitochondrial particles and by antimycin A but abolished by rotenone. Inhibition of cytochrome c oxidase activity by the adriamycin-Fe3+ complex is reversible and activity is recovered upon solubilization of the particles. |
1(0,0,0,1) | Details |
16243845 | Panov A, Dikalov S, Shalbuyeva N, Taylor G, Sherer T, Greenamyre JT: Rotenone model of Parkinson disease: multiple brain mitochondria dysfunctions after short term systemic rotenone intoxication. Nucl Med Biol. 1995 May;22(4):491-6. In Rot rat brain mitochondria (Rot-RBM) there was a 30-40% inhibition of respiration in State 3 and State 3U with Complex I substrates and |
1(0,0,0,1) | Details |
19409963 | Caudle WM, Kitsou E, Li J, Bradner J, Zhang J: A role for a novel protein, nucleolin, in Parkinson's disease. FEBS Lett. 2007 Dec 22;581(30):5803-6. Epub 2007 Nov 26. Furthermore, manipulation of nucleolin in an in vitro model of PD resulted in significant alterations in the generation of oxidative stress as well as proteasomal inhibition following rotenone exposure. |
0(0,0,0,0) | Details |
2846570 | Krishnamoorthy G, Hinkle PC: Studies on the electron transfer pathway, topography of iron- centers, and site of coupling in -Q oxidoreductase. Biochem J. 1996 Aug 15;318 ( Pt 1):343-9. N-Bromosuccinimide also destroyed the signal from N-4 but without inhibiting rotenone-sensitive electron transfer to suggesting a branched pathway for electron transfer. |
0(0,0,0,0) | Details |
15317809 | Muller FL, Liu Y, Van Remmen H: Complex III releases to both sides of the inner mitochondrial membrane. Biochem J. 1977 Jun 1;163(3):605-15. This finding fits well with the proposed site of electron leak at Complex I, namely the iron- clusters of the (matrix-protruding) hydrophilic arm. |
1(0,0,0,1) | Details |
20056551 | Mou T, Jing H, Yang W, Fang W, Peng C, Guo F, Zhang X, Pang Y, Ma Y: Preparation and biodistribution of [18F] FP2OP as myocardial perfusion imaging agent for positron emission tomography. J Biol Chem. 2004 Nov 19;279(47):49064-73. Epub 2004 Aug 17. Ex vivo autoradiography demonstrates that [(18) F] FP2OP may have high affinity with MC-I and that can be blocked by [(19) F] FP2OP or rotenone (a known MC-I inhibitor). Myocardial extractions of pyridaben, a mitochondrial complex I (MC-I) inhibitor, is well correlated with blood flow. |
1(0,0,0,1) | Details |
18786503 | Lin SS, Kerscher S, Saleh A, Brandt U, Gross U, Bohne W: The Toxoplasma gondii type-II NADH dehydrogenase TgNDH2-I is inhibited by 1- -2-alkyl-4 (1H) quinolones. Basic Res Cardiol. 2003 Mar;98(2):114-23. The apicomplexan parasite Toxoplasma gondii does not possess complex I of the mitochondrial respiratory chain, but has two genes encoding rotenone-insensitive, non- pumping type-II NADH dehydrogenases (NDH2s). |
0(0,0,0,0) | Details |
20227863 | He M, Siow RC, Sugden D, Gao L, Cheng X, Mann GE: Induction of HO-1 and redox signaling in endothelial cells by advanced glycation end products: A role for Nrf2 in vascular protection in diabetes. FEBS Lett. 1994 Oct 3;352(3):375-9. Inhibition of ROS production with the scavenger Tiron or inhibitors of flavoproteins (diphenylene iodonium) and oxidase (apocynin), but not eNOS (l-NAME) or mitochondria complex I (rotenone) abrogated HO-1 induction by AGE-BSA. |
0(0,0,0,0) | Details |
11798036 | Leverve XM, Fontaine E: Role of substrates in the regulation of mitochondrial function in situ. Nucleosides Nucleotides Nucleic Acids. 2004 Oct;23(8-9):1275-9. We then review results indicating that the activity of complex I directly regulates the PTP, a finding that emphasizes the importance of the respiratory substrates in PTP regulation. |
1(0,0,0,1) | Details |
9878531 | Li Y, Trush MA: Diphenyleneiodonium, an NAD (P) H oxidase inhibitor, also potently inhibits mitochondrial reactive species production. J Bioenerg Biomembr. 2001 Jun;33(3):251-7. DPI was as potent as rotenone in inhibiting the production of and H2O2 by mitochondrial respiration. With substrate-supported isolated mitochondria, DPI was shown to reduce mitochondrial production probably through inhibiting NADH-ubiquinone oxidoreductase (complex I). |
1(0,0,0,1) | Details |
15843045 | Tomaselli B, Podhraski V, Heftberger V, Bock G, Baier-Bitterlich G: mediated protection of chemical hypoxia-induced neuronal injuries involves p42/44 MAPK activation. Oncogene. 2005 May 26;24(23):3715-25. O (2)-sensitive neuronal pheochromocytoma (PC12)-cells, which are widely used as a model system for sympathetic ganglion-like neurons, were subjected to chemical hypoxia induced with rotenone, an inhibitor of mitochondrial complex I. O (2)-sensitive neuronal pheochromocytoma (PC12)-cells, which are widely used as a model system for sympathetic ganglion-like neurons, were subjected to chemical hypoxia induced with rotenone, an inhibitor of mitochondrial complex I. |
nucleoside-1(0,0,0,1) | Details |
8522981 | Budd SL, Nicholls DG: A reevaluation of the role of mitochondria in neuronal Ca2+ homeostasis. Antioxid Redox Signal. 1999 Fall;1(3):285-95. The further addition of the mitochondrial complex I inhibitor rotenone led to a collapse of the mitochondrial membrane potential, monitored by rhodamine-123, but had no effect on ATP/ADP ratios. |
0(0,0,0,0) | Details |
16154284 | Campanucci VA, Brown ST, Hudasek K, O'kelly IM, Nurse CA, Fearon IM: O2 sensing by recombinant TWIK-related halothane-inhibitable K+ channel-1 background K+ channels heterologously expressed in human embryonic kidney cells. Chem Res Toxicol. 2004 Nov;17(11):1540-8. Neither the mitochondrial complex I inhibitors rotenone, myxothiazol and nor the oxidase inhibitors diphenylene iodonium and phenylarsine oxide, were effective in inhibiting the O2-sensitivity of THIK-1. |
0(0,0,0,0) | Details |
15650392 | Bundy RE, Hoare GS, Kite A, Beach J, Yacoub M, Marczin N: Redox regulation of p38 MAPK activation and expression of ICAM-1 and heme oxygenase-1 in human alveolar epithelial (A549) cells. Anal Chem. 2006 Apr 1;78(7):2422-31. The mitochondrial complex I and III inhibitors, rotenone and antimycin A, and allopurinol partially inhibited H2O2- but not TNFalpha-induced p38 activation. |
0(0,0,0,0) | Details |
19488053 | Torres S, Salgado-Ceballos H, Guizar-Sahagun G, Torres JL, Orozco-Suarez S, Diaz-Ruiz A, Vazquez ME, Collado C, Rios C: Deleterious versus neuroprotective effect of metabolic inhibition after traumatic spinal cord injury. Spinal Cord. 2009 Oct;47(10):745-50. Epub 2009 Jun 2. METHODS: Animals were divided into five groups: one sham and four with TSCI, including no treatment, rotenone (inhibitor of mitochondrial complex I), azide (inhibitor of mitochondrial complex IV) and of or non-degradable cocarboxylase as a metabolic reactivator. |
0(0,0,0,0) | Details |
18234847 | Buttigieg J, Brown ST, Lowe M, Zhang M, Nurse CA: Functional mitochondria are required for O2 but not CO2 sensing in immortalized adrenomedullary chromaffin cells. Mech Ageing Dev. 2005 Apr;126(4):505-11. Epub 2004 Dec 15. Rotenone (1 microM), a mitochondrial complex I blocker known to mimic and occlude the effects of hypoxia in primary AMC, was effective in wild-type but not rho (0) MAH cells. |
0(0,0,0,0) | Details |
14732287 | Herrera B, Murillo MM, Alvarez-Barrientos A, Beltran J, Fernandez M, Fabregat I: Source of early reactive hepatocytes. J Neurochem. 2008 Apr;105(2):360-8. Epub 2007 Nov 25. Rotenone, an inhibitor of the NADH dehydrogenase in mitochondrial complex I, attenuated, but did not completely inhibit, ROS-production, caspase activation, and cell death mediated by TGF-beta. |
species in the apoptosis induced by transforming growth factor-beta in fetal rat 0(0,0,0,0) | Details |
17069748 | Belyaeva EA, Dymkowska D, Wieckowski MR, Wojtczak L: Reactive hepatoma AS-30D cells. Neuroscience. 2009 Oct 20;163(3):735-40. Epub 2009 Jul 4. Inhibitors of the mitochondrial permeability transition pore, cyclosporin A and bongkrekic acid, and inhibitors of respiratory complex III, stigmatellin and antimycin A, but not inhibitor of complex I, rotenone, partly prevented necrosis evoked by exposure of the cells to Cd (2+). |
species produced by the mitochondrial respiratory chain are involved in Cd2+-induced injury of rat ascites 0(0,0,0,0) | Details |
11370674 | Velazquez I, Pardo JP: Kinetic characterization of the rotenone-insensitive internal oxidoreductase of mitochondria from Saccharomyces cerevisiae. Biochem Biophys Res Commun. 1998 Dec 18;253(2):295-9. Due to the fact that S. cerevisiae cells lack complex I, the expression of this protein is essential for cell growth under respiratory conditions. |
1(0,0,0,1) | Details |
12226375 | Moller IM, Roberts TH, Rasmusson AG: Oxidation in Potato Tuber Mitochondria. Plant Physiol. 1996 Sep;112(1):75-78. We conclude that UQ-1-induced external deamino- oxidation is due to a change in specificity of the external rotenone-insensitive NADH dehydrogenase. |
Induces External Deamino- 0(0,0,0,0) | Details |
7767529 | Hokanson JF, Mercier JG, Brooks GA: Cyclosporine A decreases rat skeletal muscle mitochondrial respiration in vitro. J Bioenerg Biomembr. 1998 Jun;30(3):235-43. CsA inhibited maximal respiration (ADP stimulated) in the presence of and rotenone by 18.3% and in the presence of and by 34.7%. |
0(0,0,0,0) | Details |
7476912 | Garcia-Ruiz C, Colell A, Morales A, Kaplowitz N, Fernandez-Checa JC: Role of oxidative stress generated from the mitochondrial electron transport chain and mitochondrial function and activation of transcription factor nuclear factor-kappa B: studies with isolated mitochondria and rat hepatocytes. J Plant Physiol. 2006 Jul;163(8):877-82. Epub 2005 Nov 9. However, blockade of complex I or II with rotenone or thenoyltrifluoroacetone, respectively, did not result in accumulation of peroxide. |
status in loss of mitochondrial 0(0,0,0,0) | Details |
8505638 | Anderson JJ, Bravi D, Ferrari R, Davis TL, Baronti F, Chase TN, Dagani F: No evidence for altered muscle mitochondrial function in Parkinson's disease. Mol Biochem Parasitol. 1984 Oct;13(2):121-34. Likewise, activities of rotenone sensitive cytochrome c reductase, cytochrome c reductase, or cytochrome oxidase in muscle mitochondria were not significantly different between Parkinsonian and control subjects. |
0(0,0,0,0) | Details |
12091466 | Gluck M, Ehrhart J, Jayatilleke E, Zeevalk GD: Inhibition of brain mitochondrial respiration by involvement of H (2) O (2) and but not -protein-mixed disulfides. Am J Physiol Cell Physiol. 2007 Jul;293(1):C22-9. Epub 2007 Apr 11. Co-administration of desferrioxamine with H (2) O (2) had no effect on complex I-associated inhibition in intact mitochondria, but attenuated inhibition of rotenone-sensitive oxidase activity by 70% in freeze-thawed mitochondria. |
0(0,0,0,0) | Details |
20035277 | Wang T, Si Y, Shirihai OS, Si H, Schultz V, Corkey RF, Hu L, Deeney JT, Guo W, Corkey BE: Respiration in Adipocytes is Inhibited by Reactive Species. Obesity (Silver Spring). 2009 Dec 24. Importantly, the ROS scavenging role of was not affected by rotenone, an inhibitor of mitochondrial complex I. |
0(0,0,0,0) | Details |
15356189 | Starkov AA, Fiskum G, Chinopoulos C, Lorenzo BJ, Browne SE, Patel MS, Beal MF: Mitochondrial alpha-ketoglutarate dehydrogenase complex generates reactive species. Brain Res. 2009 Jul 7;1279:1-8. Epub 2009 May 13. In the absence of ADP or in the presence of rotenone, H (2) O (2) production rates correlated with the reduction level of mitochondrial with various substrates, with the exception of alpha-ketoglutarate. |
0(0,0,0,0) | Details |
16251452 | Bao L, Avshalumov MV, Rice ME: Partial mitochondrial inhibition causes striatal release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion. Biochim Biophys Acta. 2003 Dec 8;1607(2-3):79-90. We show here that acute exposure to the mitochondrial complex I inhibitor rotenone (30-100 nM; 30 min) causes concentration-dependent suppression of single-pulse evoked (DA) release monitored in real time with carbon-fiber microelectrodes in guinea pig striatal slices, with no effect on DA content. |
0(0,0,0,0) | Details |
19028798 | Yamaguchi O, Kaneshiro T, Saitoh S, Ishibashi T, Maruyama Y, Takeishi Y: Regulation of coronary vascular tone via redox modulation in the alpha1-adrenergic-angiotensin-endothelin axis of the myocardium. J Immunol Methods. 2007 Sep 30;326(1-2):76-82. Epub 2007 Aug 1. Dihydroethidium (DHE) and dichlorodihydrofluorescein (DCF) intensities were increased by stimulation in isolated rat cardiac myocytes, which were enhanced by the mitochondrial electron transport chain complex I inhibitor rotenone (DHE: 20.4 +/- 1.2-fold and DCF: 25.2 +/- 0.9-fold, n = 8, P < 0.01, respectively) but not by the oxidase inhibitor apocynin. |
0(0,0,0,0) | Details |
7763312 | Anderson WM, Trgovcich-Zacok D: Carbocyanine dyes with long alkyl side-chains: broad spectrum inhibitors of mitochondrial electron transport chain activity. J Neurochem. 2003 Jan;84(1):112-8. Certain indocarbocyanine, thiacarbocyanine, and oxacarbocyanine dyes possessing short alkyl side-chains (one to five carbons) are potent inhibitors of mammalian mitochondrial -ubiquinone reductase (EC 1.6.99.3) activity (Anderson et al., Biochem Pharmacol 41: 677-684, 1991; Anderson et al., Biochem Pharmacol 45: 691-696, 1993; Anderson et al., Biochem Pharmacol 45: 2115-2122, 1993), and act similarly to rotenone. |
0(0,0,0,0) | Details |
18945820 | Shin SM, Kim SG: Inhibition of and iron-induced mitochondrial dysfunction and apoptosis by oltipraz and novel 1,2-dithiole-3-thione congeners. Nature. 1995 Oct 5;377(6548):438-41. Oltipraz was found to attenuate apoptosis induced by rotenone (complex I inhibitor), but not that by antimycin A (complex III inhibitor), suggesting that the inhibition of AA-induced apoptosis by oltipraz might be associated with the electron transport system. |
0(0,0,0,0) | Details |
11569921 | Ishiguro H, Yasuda K, Ishii N, Ihara K, Ohkubo T, Hiyoshi M, Ono K, Senoo-Matsuda N, Shinohara O, Yosshii F, Murakami M, Hartman PS, Tsuda M: Enhancement of oxidative damage to cultured cells and Caenorhabditis elegans by mitochondrial electron transport inhibitors. Mol Pharmacol. 2009 Jan;75(1):242-53. Epub 2008 Oct 22. loading enhanced the damage of PC 12 cells by thenoyltrifluoroacetone (TTFA, a complex II inhibitor), but did not by rotenone (a complex I inhibitor), antimycin (a complex III inhibitor), and azide (a complex IV inhibitor). |
0(0,0,0,0) | Details |
4315616 | Gutman M, Singer TP, Beinert H, Casida JE: Reaction sites of rotenone, piericidin A, and amytal in relation to the nonheme iron components of NADH dehydrogenase. J Neurochem. 2008 Jul;106(2):826-34. Epub 2008 Apr 28. |
0(0,0,0,0) | Details |
12401552 | Kitamura Y, Inden M, Miyamura A, Kakimura J, Taniguchi T, Shimohama S: Possible involvement of both mitochondria- and endoplasmic reticulum-dependent caspase pathways in rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells. Chem Res Toxicol. 2004 Sep;17(9):1272-9. |
0(0,0,0,0) | Details |
8944779 | Beattie DS, Howton MM: The presence of rotenone-sensitive NADH dehydrogenase in the long slender bloodstream and the procyclic forms of Trypanosoma brucei brucei. Biochemistry. 2009 Mar 10;48(9):2053-62. |
0(0,0,0,0) | Details |
12270629 | Fang J, Beattie DS: Rotenone-insensitive NADH dehydrogenase is a potential source of in procyclic Trypanosoma brucei mitochondria. FEBS J. 2007 Jun;274(12):3150-8. Epub 2007 May 22. |
0(0,0,0,0) | Details |
8442768 | Anderson WM, Delinck DL, Benninger L, Wood JM, Smiley ST, Chen LB: Cytotoxic effect of thiacarbocyanine dyes on human colon carcinoma cells and inhibition of bovine heart mitochondrial -ubiquinone reductase activity via a rotenone-type mechanism by two of the dyes. Biochim Biophys Acta. 2002 Oct 3;1556(1):73-80. |
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15140267 | Geisler DA, Johansson FI, Svensson AS, Rasmusson AG: Antimycin A treatment decreases respiratory internal rotenone-insensitive oxidation capacity in potato leaves. Biochim Biophys Acta. 1998 May 6;1364(2):222-35. |
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11597127 | Guidarelli A, Clementi E, De Nadai C, Bersacchi R, Cantoni O: TNFalpha enhances the DNA single-strand breakage induced by the short-chain lipid hydroperoxide analogue tert-butylhydroperoxide via -dependent inhibition of complex III followed by enforced and peroxide formation. Mitochondrion. 2006 Oct;6(5):235-44. Epub 2006 Aug 3. The following lines of evidence suggest that the enhancing effects of TNFalpha are mediated by inhibition of complex III and by the ensuing formation of superoxides and peroxide: (a) the effects of TNFalpha were mimicked by the complex III inhibitor antimycin A; (b) the effects of TNFalpha, or antimycin A, were abolished by the complex I inhibitor rotenone, or by myxothiazol, an agent which inhibits the electron flow from the reduced to cytochrome c (1) and therefore prevents formation; (c) the effects of TNFalpha, or antimycin A, were not observed in respiration-deficient cells; and (d) the effects of TNFalpha, or antimycin A, were sensitive to catalase. |
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19013527 | Meurers BH, Zhu C, Fernagut PO, Richter F, Hsia YC, Fleming SM, Oh M, Elashoff D, Dicarlo CD, Seaman RL, Chesselet MF: Low dose rotenone treatment causes selective transcriptional activation of cell death related pathways in dopaminergic neurons in vivo. J Bioenerg Biomembr. 2002 Apr;34(2):89-94. |
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17951219 | Sharifpanah F, Wartenberg M, Hannig M, Piper HM, Sauer H: Peroxisome proliferator-activated receptor alpha agonists enhance cardiomyogenesis of mouse ES cells by utilization of a reactive species-dependent mechanism. Cancer Res. 1990 Dec 15;50(24):7876-81. Treatment with PPARalpha, but not PPARbeta, and PPARgamma agonists and MK886, resulted in generation of reactive species (ROS), which was inhibited in the presence of the oxidase inhibitors diphenylen iodonium (DPI) and apocynin and the free radical scavengers and N-(2-mercapto-propionyl)- (NMPG), whereas the mitochondrial complex I inhibitor rotenone was without effects. |
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18646208 | Maalouf M, Rho JM: Oxidative impairment of hippocampal long-term potentiation involves activation of protein phosphatase 2A and is prevented by ketone bodies. J Biol Chem. 2004 Nov 12;279(46):47961-7. Epub 2004 Sep 3. We found that: 1) a combination of ACA and BHB (1 mM each) prevented impairment of LTP by H (2) O (2) (200 microM); 2) KB significantly lowered intracellular levels of reactive species (ROS)--measured with the fluorescent indicator carboxy-H (2) DCFDA (carboxy-2',7'-dichlorodihydrofluorescein --in CA1 pyramidal neurons exposed to H (2) O (2); 3) the effect of KB on LTP was replicated by the protein phosphatase 2A (PP2A) inhibitor fostriecin; 4) KB prevented impairment of LTP by the PP2A activator C (6) 5) fostriecin did not prevent the increase in ROS levels in CA1 pyramidal neurons exposed to H (2) O (2), and C (6) did not increase ROS levels; 6) PP2A activity was enhanced by both H (2) O (2) and rotenone (a mitochondrial complex I inhibitor that increases endogenous production); and 7) KB inhibited PP2A activity in protein extracts from brain tissue treated with either H (2) O (2) or |
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17018646 | Ramachandiran S, Hansen JM, Jones DP, Richardson JR, Miller GW: Divergent mechanisms of paraquat, MPP+, and rotenone toxicity: oxidation of thioredoxin and caspase-3 activation. FEBS Lett. 2003 Aug 14;549(1-3):39-42. |
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18487445 | Viel EC, Benkirane K, Javeshghani D, Touyz RM, Schiffrin EL: Xanthine oxidase and mitochondria contribute to vascular generation in DOCA-salt hypertensive rats. Clin Chem. 2000 Mar;46(3):345-50. O (2)(*-) generation decreased with in situ treatment by tenoyltrifluoroacetone and CCCP, inhibitors of mitochondrial electron transport complexes II and IV, respectively, whereas rotenone (mitochondrial complex I inhibitor) had no effect. |
0(0,0,0,0) | Details |
11579170 | Leach RM, Hill HM, Snetkov VA, Robertson TP, Ward JP: Divergent roles of glycolysis and the mitochondrial electron transport chain in hypoxic pulmonary vasoconstriction of the rat: identity of the hypoxic sensor. Am J Physiol Regul Integr Comp Physiol. 2010 Apr;298(4):R1026-34. Epub 2010 Jan 20. Inhibition of complex I of the ETC with rotenone (100 nM) or complex III with myxothiazol (100 nM) did not cause vasoconstriction in normoxia, but abolished both phases of HPV. |
0(0,0,0,0) | Details |
15764673 | Bailey SR, Mitra S, Flavahan S, Flavahan NA: Reactive smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries. Brain Res Dev Brain Res. 1990 Aug 1;55(1):51-5. The inhibitor of mitochondrial complex I rotenone (10 micromol/l), the antioxidant (NAC; 20 mmol/l), or the cell-permeable mimic of superoxide dismutase MnTMPyP (50 micromol/l) did not affect vasoconstriction to alpha2-AR stimulation (UK-14304) at 37 degrees C but dramatically inhibited the response at 28 degrees C. |
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8226719 | Moller IM, Rasmusson AG, Fredlund KM: NAD (P) H-mitochondria. . J Neurosci. 2008 Dec 10;28(50):13511-21. On the outer surface, facing the intermembrane space and the cytoplasm, and are oxidized by what is probably a single low-molecular-weight, nonproton-pumping, unspecific rotenone-insensitive NAD (P) H dehydrogenase. |
oxidoreductases in plant 0(0,0,0,0) | Details |
12623788 | da Silva MM, Sartori A, Belisle E, Kowaltowski AJ: Ischemic preconditioning inhibits mitochondrial respiration, increases H2O2 release, and enhances K+ transport. Am J Physiol Heart Circ Physiol. 2003 Jul;285(1):H154-62. Epub 2003 Mar 6. Preconditioning also increased mitochondrial H2O2 release, an effect related to respiratory inhibition, because it is not observed in the presence of plus rotenone and can be mimicked by chemically inhibiting complex I in the presence of -linked substrates. |
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19129916 | Wang AL, Lukas TJ, Yuan M, Du N, Tso MO, Neufeld AH: Autophagy and exosomes in the aged retinal pigment epithelium: possible relevance to drusen formation and age-related macular degeneration. J Biol Chem. 2002 Feb 15;277(7):5411-7. Epub 2001 Nov 27. By in vitro modeling increased mtDNA damage induced by rotenone, an inhibitor of mitochondrial complex I, in the RPE, we found that the phagocytic activity was not altered but that there were: 1) increased autophagic markers, 2) decreased lysosomal activity, 3) increased exocytotic activity and 4) release of chemoattractants. |
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16186119 | Fujii N, Hirshman MF, Kane EM, Ho RC, Peter LE, Seifert MM, Goodyear LJ: AMP-activated protein kinase alpha2 activity is not essential for contraction- and hyperosmolarity-induced transport in skeletal muscle. PLoS One. 2009 Nov 18;4(11):e7878. Known AMPK stimuli including -1-beta-4-ribofuranoside rotenone (a Complex I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contraction, and (producing hyperosmolar shock) did not increase AMPK alpha2 activity in alpha2i TG mice, whereas alpha1 activation was attenuated by only 30-50%. |
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14699012 | Cherednichenko G, Zima AV, Feng W, Schaefer S, Blatter LA, Pessah IN: cardiac sarcoplasmic reticulum regulates -induced release. Free Radic Biol Med. 2008 Apr 1;44(7):1443-51. Epub 2008 Jan 11. A significant contribution by mitochondria was excluded as oxidation by SR exhibited > 9-fold higher catalytic activity (8.8 micromol/mg protein per minute) in the absence of exogenous mitochondrial complex I or complex III (cytochrome c) electron acceptors, but was inhibited by rotenone and pyridaben (IC50=2 to 3 nmol/L), antimycin A (IC50=13 nmol/L), and diphenyleneiodonium (IC50=28 micromol/L). |
oxidase activity of rat 0(0,0,0,0) | Details |
12576057 | Gostimskaya IS, Grivennikova VG, Zharova TV, Bakeeva LE, Vinogradov AD: In situ assay of the intramitochondrial enzymes: use of alamethicin for permeabilization of mitochondria. IUBMB Life. 2001 Sep-Nov;52(3-5):221-9. Alamethicin-treated mitochondria show high rotenone-sensitive oxidase, -quinone reductase, and oligomycin-sensitive and carboxyatractylate-insensitive ATPase activities. |
0(0,0,0,0) | Details |
18456002 | Liu F, Hindupur J, Nguyen JL, Ruf KJ, Zhu J, Schieler JL, Bonham CC, Wood KV, Davisson VJ, Rochet JC: Methionine sulfoxide reductase A protects dopaminergic cells from Parkinson's disease-related insults. Free Radic Biol Med. 2008 Aug 1;45(3):242-55. Epub 2008 Apr 11. Here, we show that MsrA suppresses dopaminergic cell death and protein aggregation induced by the complex I inhibitor rotenone or mutant alpha-synuclein, but not by the proteasome inhibitor MG132. |
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7840680 | Taylor DE, Ghio AJ, Piantadosi CA: Reactive liver mitochondria of rats in sepsis. . Exp Neurol. 2009 May;217(1):231-4. Epub 2009 Jan 29. Inhibition of electron transport at Complex I with rotenone had no effect on this pattern of OH. production, but rotenone and abolished the differences in OH. formation between control and septic liver mitochondria. |
species produced by 0(0,0,0,0) | Details |
11741286 | Armstrong JS, Hornung B, Lecane P, Jones DP, Knox SJ: Rotenone-induced G2/M cell cycle arrest and apoptosis in a human B lymphoma cell line PW. Tsitologiia. 2004;46(11):985-92. |
0(0,0,0,0) | Details |
12130563 | Hsieh TJ, Zhang SL, Filep JG, Tang SS, Ingelfinger JR, Chan JS: High glucose stimulates angiotensinogen gene expression via reactive species generation in rat kidney proximal tubular cells. Endocrinology. 2002 Aug;143(8):2975-85. These effects of high were blocked by antioxidants and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived transport into mitochondria (alpha-cyano- an uncoupler of oxidative phosphorylation (carbonyl m-chlorophenylhydrazone), a manganese superoxide dismutase mimetic, catalase, and a specific inhibitor of p38 MAPK (SB 203580), but were not affected by an inhibitor of the - shuttle (aminooxyacetate acid). |
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11239497 | Guo Q, Tirosh O, Packer L: Inhibitory effect of and its positively charged amide analogue on production in RAW 264.7 macrophages. Exp Neurol. 2007 Oct;207(2):218-26. Epub 2007 Jun 29. Furthermore, in the presence of 2.5 or 25 mM the inhibitory effects of R (+) LA and R (+) LA-plus on NO production were decreased markedly, while they showed more potent inhibitory effects in the presence of 2 microM rotenone or 5 microg/mL of antimycin A, inhibitors of mitochondrial complex I and complex III, respectively. |
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19232048 | Tarasenko VI, Garnik EY, Shmakov VN, Konstantinov YM: Induction of Arabidopsis gdh2 gene expression during changes in redox state of the mitochondrial respiratory chain. Biochem J. 1988 Aug 15;254(1):303-5. Inhibition of complex I by rotenone did not influence the transcript level, but treatment with a complex IV inhibitor, also increased the transcript content. |
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