Protein Information

Name catalase
Synonyms CAT; Catalase; Erythrocyte derived growth promoting factor; Carnitine O acetyltransferase; Carnitine acetylase; Carnitine acetyltransferase; CAT; Catalases…

Compound Information

Name rotenone
CAS

Reference List

PubMed Abstract RScore(About this table)
3843927 Briskin DP, Thornley WR, Poole RJ: Vanadate-dependent NADH oxidation in microsomal membranes of sugar beet. Arch Biochem Biophys. 1985 Jan;236(1):228-37.

The oxidation activity was insensitive to rotenone and antimycin A but was inhibited by NaN3, NaCN, and quinacrine.
Catalase prevented Na3VO4-dependent O2 consumption but accelerated NADH oxidation.
2(0,0,0,2) Details
12821678 Hua H, Munk S, Goldberg H, Fantus IG, Whiteside CI: High glucose-suppressed endothelin-1 Ca2+ signaling via NADPH oxidase and diacylglycerol-sensitive protein kinase C isozymes in mesangial cells. J Biol Chem. 2003 Sep 5;278(36):33951-62. Epub 2003 Jun 23.

Likewise, catalase or p47phox antisense oligonucleotide normalized the [Ca2+] i response to ET-1 in HG to 521 +/- 58 nM and 514 +/- 48 nM, respectively.
Pretreatment with carbonyl cyanide m-chlorophenylhydrazone or rotenone did not restore Ca2+ signaling in HG.
2(0,0,0,2) Details
9144655 Horakova L, Stolc S, Chromikova Z, Pekarova A, Derkova L: Mechanisms of hippocampal reoxygenation injury. Neuropharmacology. 1997 Feb;36(2):177-84.

The injury induced by a hypoxia of 12 min and reoxygenation was reduced by SOD and catalase, indicating that oxygen radicals were involved in this process.
The oxygen radicals originating from the xanthine/xanthine oxidase system, from the synthesis of prostaglandins, as well as from the mitochondrial respiratory chain, since allopurinol, indomethacin and rotenone decreased while antimycin increased reoxygenation injury.
1(0,0,0,1) Details
11121805 Hsieh CC, Yen MH, Yen CH, Lau YT: Oxidized low density lipoprotein induces apoptosis via generation of reactive oxygen species in vascular smooth muscle cells. Cardiovasc Res. 2001 Jan;49(1):135-45.

Since oxLDL-induced ROS generation were inhibited by nordihydroguaiaretic acid and rotenone, lipoxygenase and mitochondrial pathways could be involved.
Catalase and deferoxamine reduced both oxLDL-induced apoptosis and ROS generation.
2(0,0,0,2) Details
3593796 Kolesova GM, Kapitanova NG, Iaguzhinskii LS: [Stimulation by quinones of cyanide-resistant respiration in rat liver and heart mitochondria]. Biokhimiia. 1987 May;52(5):715-9.

Rotenone and antimycin A do not inhibit the cyanide-resistant respiration.
Superoxide dismutase, Cu2+ and catalase inhibit the CN-resistant respiration in the presence of quinones.
2(0,0,0,2) Details
16661630 Salin ML, Bridges SM: Chemiluminescence in Wounded Root Tissue : EVIDENCE FOR PEROXIDASE INVOLVEMENT. Plant Physiol. 1981 Jan;67(1):43-46.

Light emission was diminished by CN (-) and N (3) (-) but was not affected by rotenone and antimycin A.
Catalase quenched chemiluminescence in wounded root segments as did ascorbic acid and hydroquinone.
1(0,0,0,1) Details
10611491 Catisti R, Vercesi AE: The participation of pyridine nucleotides redox state and reactive oxygen in the fatty acid-induced permeability transition in rat liver mitochondria. FEBS Lett. 1999 Dec 24;464(1-2):97-101.

This second phase of DeltaPsi dissipation could also be prevented by rotenone or NAD (P) H-linked substrates which decrease the pyridine nucleotide (PN) oxidation that follows the stimulation of oxygen consumption induced by AA or FCCP.
Exogenous catalase also inhibited both AA- and FCCP-induced PTP opening.
1(0,0,0,1) Details
2914918 Mihalik SJ, Rhead WJ: L-pipecolic acid oxidation in the rabbit and cynomolgus monkey. J Biol Chem. 1989 Feb 15;264(5):2509-17.

When monkey kidney cortex was fractionated on Percoll gradients, L-pipecolic acid oxidation activity paralleled that of the peroxisomal marker, catalase.
Activity was inhibited by both rotenone and antimycin A and was maximal when FAD, phenazine ethosulfate, and glycerol were included in the assay; Km,app was 0.74 +/- 0.16 mM.
1(0,0,0,1) Details
1854636 Han YH, Smibert RM, Krieg NR: Wolinella recta, Wolinella curva, Bacteroides ureolyticus, and Bacteroides gracilis are microaerophiles, not anaerobes. Int J Syst Bacteriol. 1991 Apr;41(2):218-22.


Catalase added to brucella broth enhanced growth.
1(0,0,0,1) Details
12673769 Bai Z, Harvey LM, McNeil B: Physiological responses of chemostat cultures of Aspergillus niger (B1-D) to simulated and actual oxidative stress. Biotechnol Bioeng. 2003 Jun 20;82(6):691-701.

Changes in the levels of intracellular superoxide anions and defensive enzyme activities, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), were monitored, together with glutathione and respiratory activity in both the dynamic phase and when a new steady state was established.
Under these conditions, it was noted that the ratio of rotenone-insensitive/total respiration increased, suggesting increased activity of the alternative respiratory pathway.
1(0,0,0,1) Details
15059640 Aitken RJ, Ryan AL, Baker MA, McLaughlin EA: Redox activity associated with the maturation and capacitation of mammalian spermatozoa. Free Radic Biol Med. 2004 Apr 15;36(8):994-1010.

This activity was suppressed by inhibitors of plasma membrane redox systems such as diphenylene iodonium, p-chloromercuribenzenesulfonic acid, and capsaicin, but was resistant to inhibition by resiniferatoxin and rotenone.
The luminol-peroxidase signal was dependent on the presence of bicarbonate, enhanced by the substitution of fructose for glucose, and severely suppressed by desferoxamine, superoxide dimutase, and catalase.
1(0,0,0,1) Details
2039603 de Groot H, Brecht M: Reoxygenation injury in rat hepatocytes: mediation by O2/H2O2 liberated by sources other than xanthine oxidase. Biol Chem Hoppe Seyler. 1991 Jan;372(1):35-41.

From the inhibitors of the mitochondrial respiratory chain, both cyanide and antimycin A increased injury while rotenone was without significant effect on injury.
When added together, superoxide dismutase and catalase completely prevented reoxygenation injury.
1(0,0,0,1) Details
16120275 Paradies G, Petrosillo G, Pistolese M, Ruggiero FM: Reactive oxygen species generated by the mitochondrial respiratory chain affect the complex III activity via cardiolipin peroxidation in beef-heart submitochondrial particles. Mitochondrion. 2001 Aug;1(2):151-9.

ROS were produced by treatment of nicotinamide adenine dinucleotide (NADH) respiring SMP with rotenone.
Both these effects were completely abolished by SOD + catalase.
1(0,0,0,1) Details
20203294 Ranzato E, Biffo S, Burlando B: Selective Ascorbate Toxicity to Malignant Mesothelioma: A Redox Trojan Mechanism. Am J Respir Cell Mol Biol. 2010 Mar 4.

Toxicity was markedly reduced by the H2O2-degrading enzyme catalase.
Two inhibitors of cellular superoxide sources, apocynin and rotenone, reduced ascorbate cytotoxicity and the ascorbate-induced rise in rhodamine fluorescence.
1(0,0,0,1) Details
10712386 Pueyo ME, Gonzalez W, Nicoletti A, Savoie F, Arnal JF, Michel JB: Angiotensin II stimulates endothelial vascular cell adhesion molecule-1 via nuclear factor-kappaB activation induced by intracellular oxidative stress. Arterioscler Thromb Vasc Biol. 2000 Mar;20(3):645-51.

In contrast, rotenone and antimycin, 2 inhibitors of the mitochondrial respiratory chain, inhibited the Ang II-induced IkappaB degradation, showing that generation of reactive oxygen species in the mitochondria is involved on Ang II action.
BXT-51702, a glutathione peroxidase mimic, inhibited the effect of Ang II, and aminotriazole, an inhibitor of catalase, enhanced it, suggesting a role for H (2) O (2) in IkappaB degradation.
1(0,0,0,1) Details
12187333 Chen SY, Lu FJ, Gau RJ, Yang ML, Huang TS: 15-Deoxy-delta12,14-prostaglandin J2 induces apoptosis of a thyroid papillary cancer cell line (CG3 cells) through increasing intracellular iron and oxidative stress. Anticancer Drugs. 2002 Aug;13(7):759-65.

Mitochondrial oxidative phosphorylation inhibitors (carbonyl cyanide m-chloro-phenylhydrazone, oligomycin, cyclosporin A and rotenone), NADPH oxidase inhibitor (diphenyleneiodonium), xanthine oxidase inhibitor (allopurinol) and NO synthase inhibitor (N-monomethyl-L-arginine acetate) did not reduce the generation of ROS.
However, catalase, N-acetyl-cysteine and the iron chelator desferri-oxamine decreased the intracellular ROS of 15d-PGJ2-treated CG3 cells.
1(0,0,0,1) Details
9586799 Tsai MJ, Lee EH: Nitric oxide donors protect cultured rat 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.
Notably, catalase, dimethyl sulfoxide and ferricyanide, an extracellular electron acceptor, were also effective in inhibiting MPP+ damage.
1(0,0,0,1) 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. Neuroscience. 2007 Mar 2;145(1):130-41. Epub 2007 Jan 4.

In whole-cell recordings, hypoxia (PO2=5-15 mm Hg) inhibited outward current in neonatal AMC; this response was reversed by exogenous H2O2 and mimicked and occluded by intracellular catalase (1000 units/ml), as well as the antioxidants, N-acetyl-L-cysteine (NAC; 50 microM) and Trolox (200 microM).
1(0,0,0,1) Details
8394729 Silva JM, O'Brien PJ: Molecular mechanisms of SR 4233-induced hepatocyte toxicity under aerobic versus hypoxic conditions. Br J Cancer. 1993 Sep;68(3):484-91.

The increased respiration was inhibited by the respiratory inhibitors KCN and antimycin A but not by rotenone.
SR 4233 however induced cyanide-resistant respiration, an indicator of redox cycling mediated oxidative stress and became cytotoxic if hepatocyte catalase or glutathione reductase was inactivated.
1(0,0,0,1) Details
7389037 Jacobson B, Biaglow JE, Fielden EM, Adams GE: Respiratory effects and ascorbate reactions with misonidazole and other recently developed drugs. Cancer Clin Trials. 1980 Spring;3(1):47-53.

Various inhibitors of electron transfer reactions, such as rotenone, antimycin A, and sodium azide, had no effect on misonidazole-stimulated oxygen utilization.
However, cyanide was found to be stimulating in this system and this may be due to the inhibition of enzymes such as catalase and superoxide dismutase known to be present in S9.
1(0,0,0,1) Details
17303708 Starnes JW, Barnes BD, Olsen ME: Exercise training decreases rat heart mitochondria free radical generation but does not prevent Ca2+-induced dysfunction. J Appl Physiol. 2007 May;102(5):1793-8. Epub 2007 Feb 15.

Rotenone, which blocks electron flow from succinate to complex 1, reduced H (2) O (2) production and eliminated differences between ET and Sed.
Catalase activity was extremely low but increased 49% in ET (P < 0.05).
1(0,0,0,1) Details
15479985 Ichikawa H, Kokura S, Aw TY: Role of endothelial mitochondria in oxidant production and modulation of neutrophil adherence. J Vasc Res. 2004 Sep-Oct;41(5):432-44. Epub 2004 Oct 12.

Blockade of electron transport in antimycin A and A/R exposed cells with rotenone, amytal or thenoyltrifluoroacetate, but not myxothiazol, prevented neutrophil adhesion, confirming a role for mitochondrial ROS.
Catalase inhibited phase 1 adhesion, indicating H (2) O (2) involvement.
1(0,0,0,1) Details
17291988 Wang QS, Zheng YM, Dong L, Ho YS, Guo Z, Wang YX: Role of mitochondrial reactive oxygen species in hypoxia-dependent increase in intracellular calcium in pulmonary artery myocytes. Free Radic Biol Med. 2007 Mar 1;42(5):642-53. Epub 2006 Dec 14.

Glutathione peroxidase-1 (Gpx1) or catalase gene overexpression to enhance H2O2 removal remarkably reduced hypoxic increases in [ROS] i and [Ca2+] i, whereas Gpx1 gene deletion had the opposite effect.
Moreover, H2O2 (5.1 microM) reversed the inhibition of the hypoxia-induced increase in [Ca2+] i by rotenone.
1(0,0,0,1) Details
16251452 Bao L, Avshalumov MV, Rice ME: Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion. J Neurosci. 2005 Oct 26;25(43):10029-40.

Confirming an essential role for H2O2, the inhibition of DA release by rotenone was prevented by catalase, a peroxide-scavenging enzyme.
112(1,2,2,2) Details
18772240 Herlein JA, Fink BD, O'Malley Y, Sivitz WI: Superoxide and respiratory coupling in mitochondria of insulin-deficient diabetic rats. Endocrinology. 2009 Jan;150(1):46-55. Epub 2008 Sep 4.


Catalase was significantly up-regulated in muscle and heart tissue and in heart mitochondria, whereas glutathione peroxidase expression was increased in liver mitochondria of diabetic rats.
1(0,0,0,1) Details
6289887 Bindoli A, Cavallini L, Jocelyn P: Mitochondrial lipid peroxidation by cumene hydroperoxide and its prevention by succinate. Biochim Biophys Acta. 1982 Sep 15;681(3):496-503.

Mitochondrial lipid peroxidation by cumene hydroperoxide is strongly inhibited by SKF52A (an inhibitor of cytochrome P-450), by antioxidants and to a lesser extent by the enzymes superoxide dismutase and catalase.
Conversely, rotenone and N-ethylmaleimide stimulate the reaction.
1(0,0,0,1) Details
6525365 Koshkin VV: [Formation of hydrogen peroxide in the mitochondria of skeletal muscles] . Biokhimiia. 1984 Nov;49(11):1908-11.

The generation of H2O2 in skeletal muscle mitochondria during the oxidation of NAD-dependent substrates and succinate is initiated by antimycin A but not by rotenone, which points to H2O2 formation at the respiratory chain site between the rotenone and antimycin blocks.
Heart and skeletal muscle mitochondria appeared to have the similar values of Vmax for H2O2 production; the catalase activity in skeletal muscle mitochondria is much lower.
1(0,0,0,1) Details
19339632 Huang S, Zhang A, Ding G, Chen R: Aldosterone-induced mesangial cell proliferation is 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-l-cysteine, catalase, SOD, mitochondrial respiratory chain complex I inhibitor rotenone (Rot), NADPH oxidase inhibitor apocynin, and DPI significantly inhibited Aldo-stimulated MC proliferation as well as EGFR transactivation.
81(1,1,1,1) Details
16378625 Wu CC, Hsu MC, Hsieh CW, Lin JB, Lai PH, Wung BS: Upregulation of heme oxygenase-1 by Epigallocatechin-3-gallate via the phosphatidylinositol 3-kinase/Akt and ERK pathways. Life Sci. 2006 May 15;78(25):2889-97. Epub 2005 Dec 27.

The inhibition of intracellular ROS production by N-acetylcysteine (NAC), glutathione (GSH), superoxide dismutase (SOD), catalase and the mitochondrial complex I inhibitor, rotenone, results in a decrease in EGCG-dependent HO-1 expression.
81(1,1,1,1) Details
6299966 Danley DL, Hilger AE, Winkel CA: Generation of hydrogen peroxide by Candida albicans and influence on murine polymorphonuclear leukocyte activity. Infect Immun. 1983 Apr;40(1):97-102.

Iodination by fungi with lactoperoxidase was reduced when blastoconidia were incubated at 25 degrees C or in the presence of catalase and the metabolic inhibitors rotenone, antimycin A, and 2-deoxyglucose.
81(1,1,1,1) Details
15677311 Rhyu DY, Yang Y, Ha H, Lee GT, Song JS, Uh ST, Lee HB: Role of reactive oxygen species in TGF-beta1-induced mitogen-activated protein kinase activation and epithelial-mesenchymal transition in renal tubular epithelial cells. J Am Soc Nephrol. 2005 Mar;16(3):667-75. Epub 2005 Jan 26.

Growth-arrested and synchronized NRK-52E cells were stimulated with TGF-beta1 (0.2 to 20 ng/ml) or H (2) O (2) (1 to 500 microM) in the presence or absence of antioxidants (N-acetylcysteine or catalase), inhibitors of NADPH oxidase (diphenyleneiodonium and apocynin), mitochondrial electron transfer chain subunit I (rotenone), and MAPK (PD 98059, an MEK [MAP kinase/ERK kinase] inhibitor, or p38 MAPK inhibitor) for up to 96 h.
31(0,1,1,1) Details
1540380 Kinnula VL, Whorton AR, Chang LY, Crapo JD: Regulation of hydrogen peroxide generation in cultured endothelial cells. . Am J Respir Cell Mol Biol. 1992 Feb;6(2):175-82.

Extracellular H2O2 generation was determined spectrofluorometrically using 3-methoxy-4-hydroxy phenylacetic acid, and intracellular H2O2 production (in or near peroxisomes) was measured indirectly using aminotriazole, which inactivates catalase in the presence of H2O2.
Furthermore, inhibition of the mitochondrial respiratory chain (rotenone, antimycin A) or microsomal cytochrome P-450 (8-methoxypsoralen) did not change extracellular H2O2 release or intracellular H2O2 production (at peroxisomes) by endothelial cells or cells in which glutathione reductase was inactivated.
4(0,0,0,4) Details
16778190 Kim YM, Kim KE, Koh GY, Ho YS, Lee KJ: Hydrogen peroxide produced by angiopoietin-1 mediates angiogenesis. Cancer Res. 2006 Jun 15;66(12):6167-74.

We found that human umbilical vein endothelial cells treated with Ang1 produce ROS transiently, which was suppressed by NADPH oxidase inhibitor, diphenylene-iodonium chloride, and rotenone.
The Ang1-induced ROS was identified as hydrogen peroxide (H2O2) using adenovirus-catalase infection.
3(0,0,0,3) Details
7775420 Gonzalez-Flecha B, Demple B: Metabolic sources of hydrogen peroxide in aerobically growing Escherichia coli. J Biol Chem. 1995 Jun 9;270(23):13681-7.

Compounds that block electron transport at NADH dehydrogenase (rotenone) or between ubiquinone and cytochrome b (antimycin) showed that univalent reduction of O2 can occur at these sites in vivo to form superoxide anion (O2-), in agreement with reports for mammalian mitochondria.
In the strains defective in respiratory chain components, catalase activity was regulated to compensate for changes in the H2O2 production rates, which maintained intracellular H2O2 at 0.1-0.2 microM during aerobic growth over a wide range of cell densities.
2(0,0,0,2) Details
17023676 Saitoh S, Zhang C, Tune JD, Potter B, Kiyooka T, Rogers PA, Knudson JD, Dick GM, Swafford A, Chilian WM: Hydrogen peroxide: a feed-forward dilator that couples myocardial metabolism to coronary blood flow. Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2614-21. Epub 2006 Oct 5.

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.
Aliquots of buffer from paced myocytes produced vasodilation of isolated arterioles (peak response 67+/-8% percent of maximal dilation) that was significantly reduced by catalase (5+/-0.5%, P <0.05) or the antagonist of Kv channels, 4-aminopyridine (18+/-4%, P <0.05).
2(0,0,0,2) Details
15561720 Ahmad IM, Aykin-Burns N, Sim JE, Walsh SA, Higashikubo R, Buettner GR, Venkataraman S, Mackey MA, Flanagan SW, Oberley LW, Spitz DR: Mitochondrial O2*- and H2O2 mediate glucose deprivation-induced stress in human cancer cells. J Biol Chem. 2005 Feb 11;280(6):4254-63. Epub 2004 Nov 23.

The hypothesis that glucose deprivation-induced cytotoxicity in transformed human cells is mediated by mitochondrial O2*- and H2O2 was first tested by exposing glucose-deprived SV40-transformed human fibroblasts (GM00637G) to electron transport chain blockers (ETCBs) known to increase mitochondrial O2*- and H2O2 production (antimycin A (AntA), myxothiazol (Myx), or rotenone (Rot)).
In the absence of ETCBs, aminotriazole-mediated inactivation of catalase in PC-3 cells demonstrated increases in intracellular steady-state levels of H2O2 during glucose deprivation.
2(0,0,0,2) Details
8005529 Llesuy S, Evelson P, Gonzalez-Flecha B, Peralta J, Carreras MC, Poderoso JJ, Boveris A: Oxidative stress in muscle and liver of rats with septic syndrome. . Free Radic Biol Med. 1994 Apr;16(4):445-51.

The rate of H2O2 production of muscle mitochondria after 12 h of sepsis with either malate-glutamate or succinate as substrates was increased about 2.5 times but was not affected when assayed in the presence of as rotenone and antimycin.
The activities of muscle antioxidant enzymes were found maximally diminished after 12 h of sepsis: 46% decrease for Mn-superoxide dismutase, 83% decrease for catalase, and 55% decrease for glutathione peroxidase.
2(0,0,0,2) Details
15913578 Sato H, Sato M, Kanai H, Uchiyama T, Iso T, Ohyama Y, Sakamoto H, Tamura J, Nagai R, Kurabayashi M: Mitochondrial reactive oxygen species and c-Src play a critical role in hypoxic response in vascular smooth muscle cells. Cardiovasc Res. 2005 Sep 1;67(4):714-22.

Catalase, a scavenger of H2O2, inhibited the hypoxia-induced ROS generation and PAI-1 gene expression.
Ablation of mitochondrial respiration by rotenone abolished hypoxia-induced ROS generation, c-Src phosphorylation, HIF-1alpha protein expression, and PAI-1 gene expression.
1(0,0,0,1) Details
19266051 Li Y, Shen H, Zhu H, Trush MA, Jiang M, Wang G: In situ real-time chemiluminescence imaging of reactive oxygen species formation from cardiomyocytes. Int J Biomed Imaging. 2008;2008:941729. Epub 2009 Feb 25.

The CL responses were completely abolished in the presence of superoxide dismutase and catalase, suggesting the primary involvement of superoxide and hydrogen peroxide (H (2) O (2)).
In contrast to BPQ-mediated redox cycling, blockage of mitochondrial electron transport chain by either antimycin A or rotenone exerted marginal effects on the ROS formation by cultured H9c2 cells.
1(0,0,0,1) Details
15958286 del Arenal IP, Rubio ME, Ramirez J, Rendon JL, Escamilla JE: Cyanide-resistant respiration in Taenia crassiceps metacestode (cysticerci) is explained by the H2O2-producing side-reaction of respiratory complex I with O2. Parasitol Int. 2005 Sep;54(3):185-93.

Bovine catalase and horse heart cytochrome c prevented the production and/or accumulation of H2O2.
Mitochondrial respiration with NADH as substrate was partially inhibited by rotenone, cyanide and antimycin in decreasing order of effectiveness.
1(0,0,0,1) Details
2717271 Mihalik SJ, Moser HW, Watkins PA, Danks DM, Poulos A, Rhead WJ: Peroxisomal L-pipecolic acid oxidation is deficient in liver from Zellweger syndrome patients. Pediatr Res. 1989 May;25(5):548-52.


L-Pipecolic acid oxidation was not inhibited by antimycin A and rotenone and produced H2O2, consistent with its involving a peroxisomal oxidase.
0(0,0,0,0) 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. Neurochem Int. 2000 May;36(6):483-8.

The effect of H2O2 on delta (psi) m in the presence of the complex I inhibitor, rotenone, was also unaltered by addition of catalase.
33(0,1,1,3) Details
17390063 Choi KM, Kang CM, Cho ES, Kang SM, Lee SB, Um HD: Ionizing radiation-induced micronucleus formation is mediated by reactive oxygen species that are produced in a manner dependent on mitochondria, Nox1, and JNK. Oncol Rep. 2007 May;17(5):1183-8.

IR also activated c-Jun N-terminal kinase (JNK), which was reversed by catalase, rotenone, or Nox1 RNA interference.
32(0,1,1,2) Details
1449272 Kumar S, Tripathi LM, Sagar P: Oxido-reductive functions of Entamoeba histolytica in relation to virulence. Ann Trop Med Parasitol. 1992 Jun;86(3):239-48.

Conversion of the dye to formazan was strongly inhibited by -SH blocking agents, but was not influenced by rotenone and antimycin A.
The activity was also inhibited by H2O2, but stimulated by catalase.
1(0,0,0,1) Details
15086456 Lee HB, Yu MR, Song JS, Ha H: Reactive oxygen species amplify protein kinase C signaling in high glucose-induced fibronectin expression by human peritoneal mesothelial cells. Kidney Int. 2004 Apr;65(4):1170-9.

Antioxidants trolox and catalase inhibited high glucose- and PMA-induced fibronectin mRNA and protein expression.
NADPH oxidase inhibitors (diphenyleneiodinium and apocynin) and an inhibitor of mitochondrial electron transport chain subunit I (rotenone) all effectively inhibited high glucose-induced cellular ROS generation and fibronectin secretion.
1(0,0,0,1) Details
11510845 Jung SK, Trimarchi JR, Sanger RH, Smith PJ: Development and application of a self-referencing glucose microsensor for the measurement of glucose consumption by pancreatic beta-cells. Anal Chem. 2001 Aug 1;73(15):3759-67.

Consumption was decreased after the application of 10 microM rotenone by 74 +/- 5% (mean +/- SEM, n = 4).
The addition of catalase to the bulk medium was shown to ameliorate surface-dependent flux distortion close to specimens, suggesting an underlying local accumulation of hydrogen peroxide.
1(0,0,0,1) Details
12130563 Hsieh TJ, Zhang SL, Filep JG, Tang SS, Ingelfinger JR, Chan JS: High glucose stimulates angiotensinogen gene expression via reactive oxygen species generation in rat kidney proximal tubular cells. Endocrinology. 2002 Aug;143(8):2975-85.

These effects of high glucose were blocked by antioxidants (taurine and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived pyruvate transport into mitochondria (alpha-cyano-4-hydroxycinnamic acid), an uncoupler of oxidative phosphorylation (carbonyl cyanide 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 malate-aspartate shuttle (aminooxyacetate acid).
Hydrogen peroxide (>/=10 (-5) M) also stimulated p38 MAPK phosphorylation, ANG secretion, and ANG mRNA gene expression, but its stimulatory effect was blocked by catalase and SB 203580.
1(0,0,0,1) Details
11929863 Zhang HJ, Zhao W, Venkataraman S, Robbins ME, Buettner GR, Kregel KC, Oberley LW: Activation of matrix metalloproteinase-2 by overexpression of manganese superoxide dismutase in human breast cancer MCF-7 cells involves reactive oxygen species. J Biol Chem. 2002 Jun 7;277(23):20919-26. Epub 2002 Apr 2.

Treatment of MCF-7 cells with antimycin A or rotenone increased intracellular ROS production and MMP-2 activation simultaneously.
A decrease in ROS by ebselen, a glutathione peroxidase mimetic, or by transduction of adenovirus containing human catalase or glutathione peroxidase cDNA abolished the effect of MnSOD on MMP-2 activation.
1(0,0,0,1) Details
15111505 Ceolotto G, Bevilacqua M, Papparella I, Baritono E, Franco L, Corvaja C, Mazzoni M, Semplicini A, Avogaro A: Insulin generates free radicals by an NAD (P) H, phosphatidylinositol 3'-kinase-dependent mechanism in human skin fibroblasts ex vivo. Diabetes. 2004 May;53(5):1344-51.


Furthermore, insulin-induced O (2)(-) production was attenuated by the NAD (P) H inhibitor apocynin, but not by rotenone or oxypurinol.
0(0,0,0,0) 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. Am J Physiol Regul Integr Comp Physiol. 2010 Apr;298(4):R1026-34. Epub 2010 Jan 20.


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).
0(0,0,0,0) Details
14627438 Guidarelli A, Fiorani M, Cantoni O: Enhancing effects of intracellular ascorbic acid on peroxynitrite-induced U937 cell death are mediated by mitochondrial events resulting in enhanced sensitivity to peroxynitrite-dependent inhibition of complex III and formation of hydrogen peroxide. Biochem J. 2004 Mar 15;378(Pt 3):959-66.

First, DHA, as well as bona fide complex III inhibitors, similarly enhanced toxicity and subsequent formation of H2O2 induced by ONOO- via a rotenone- or catalase-sensitive mechanism.
31(0,1,1,1) Details
17635749 Ho C, Lee PH, Huang WJ, Hsu YC, Lin CL, Wang JY: Methylglyoxal-induced fibronectin gene expression through Ras-mediated NADPH oxidase activation in renal mesangial cells. Nephrology. 2007 Aug;12(4):348-56.

METHODS: Rat kidney mesangial cells with or without pretreatment with inhibitors, including superoxide dismutase, catalase, L-NAME, diphenylene iodonium, rotenone, allopurinol, PD98059, SB203580 and SP600125 were cultured in medium containing 100 microM MGO.
31(0,1,1,1) Details
8403080 Snyder JW, Alexander GM, Ferraro TN, Grothusen JR, Farber JL: N-methyl-4-phenylpyridinium (MPP+) potentiates the killing of cultured hepatocytes by catecholamines. Chem Biol Interact. 1993 Sep;88(2-3):209-23.

The participation of activated oxygen species in the cell injury under such circumstances was shown by the ability of catalase and the ferric iron chelator deferoxamine to protect the hepatocytes.
The toxicity of catecholamines was also potentiated by the mitochondrial site I (NADH dehydrogenase) inhibitor rotenone.
1(0,0,0,1) Details
15312158 Maciel EN, Kowaltowski AJ, Schwalm FD, Rodrigues JM, Souza DO, Vercesi AE, Wajner M, Castilho RF: Mitochondrial permeability transition in neuronal damage promoted by Ca2+ and respiratory chain complex II inhibition. J Neurochem. 2004 Sep;90(5):1025-35.


ADP, cyclosporin A and catalase prevented or delayed this effect, indicating it is mediated by reactive oxygen species and mitochondrial permeability transition (PT).
1(0,0,0,1) Details
3647757 Coulombe RA Jr, Briskin DP, Keller RJ, Thornley WR, Sharma RP: Vanadate-dependent oxidation of pyridine nucleotides in rat liver microsomal membranes. Arch Biochem Biophys. 1987 Jun;255(2):267-73.

Sodium vanadate-dependent oxidation of NADH was inhibited by rotenone, antimycin A, NaN3, and NaCN.
Vanadate-dependent oxidation of either pyridine nucleotide was inhibited by the addition of either superoxide dismutase or catalase, indicating that both superoxide and hydrogen peroxide may be intermediates in the process.
1(0,0,0,1) Details
15986371 Remans PH, van Oosterhout M, Smeets TJ, Sanders M, Frederiks WM, Reedquist KA, Tak PP, Breedveld FC, van Laar JM: Intracellular free radical production in synovial T lymphocytes from patients with rheumatoid arthritis. Arthritis Rheum. 2005 Jul;52(7):2003-9.

One of the ROS involved appeared to be H2O2, since catalase suppressed intracellular ROS production.
Superoxide dismutase, which uses superoxide as a substrate to form H2O2, diphenyleneiodonium (an inhibitor of NADPH oxidase), N (G)-monomethyl-L-arginine (an inhibitor of nitric oxide synthesis), nordihydroguaiaretic acid (an inhibitor of lipoxygenase), and rotenone (an inhibitor of mitochondrial ROS production) failed to suppress ROS production.
1(0,0,0,1) Details
15255947 Vesce S, Kirk L, Nicholls DG: Relationships between superoxide levels and delayed calcium deregulation in cultured cerebellar granule cells exposed continuously to glutamate. J Neurochem. 2004 Aug;90(3):683-93.


Oxidative stress of mitochondrial origin is readily detectable, as the inhibitors rotenone and antimycin A markedly increase superoxide levels with no effect on cytoplasmic-free Ca2+.
0(0,0,0,0) Details
9266505 Ruuge EK, Kashkarov KP, Lakomkin VL, Timoshin AA, Vasil'eva EV: The redox state of coenzyme Q10 in mitochondrial respiratory chain and oxygen-derived free radical generation in cardiac cells. Mol Aspects Med. 1997;18 Suppl:S41-50.


The spin-trapping experiments with TEMPONE-H showed that the rate of oxyradical generation in isolated cardiomyocytes essentially increased after hypoxia or on adding rotenone and antimycin A.
0(0,0,0,0) Details
19729059 Mendez-Samperio P, Perez A, Torres L: Role of reactive oxygen species (ROS) in Mycobacterium bovis bacillus Calmette Guerin-mediated up-regulation of the human cathelicidin LL-37 in A549 cells. Microb Pathog. 2009 Nov;47(5):252-7. Epub 2009 Sep 1.

Moreover, M. bovis BCG-mediated cathelicidin LL-37 mRNA expression was significantly blocked by the effect of the mitochondrial electron transfer chain subunit I inhibitor rotenone and H (2) O (2) scavenging enzyme catalase.
31(0,1,1,1) Details
15904944 Molina-Jimenez MF, Sanchez-Reus MI, Cascales M, Andres D, Benedi J: Effect of fraxetin on antioxidant defense and stress proteins in human neuroblastoma cell model of rotenone neurotoxicity. Toxicol Appl Pharmacol. 2005 Dec 15;209(3):214-25.

Thus, these considerations prompted us to investigate the way in which fraxetin and myricetin affect the endogenous antioxidant defense system, such as Mn and CuZn superoxide dismutase (MnSOD, CuZnSOD), catalase, glutathione reductase (GR), and glutathione peroxidase (GPx) on rotenone neurotoxicity in neuroblastoma cells.
18(0,0,3,3) 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: Sulforaphane-induced cell death in human prostate cancer cells is initiated by reactive oxygen species. J Biol Chem. 2005 May 20;280(20):19911-24. Epub 2005 Mar 11.

All these effects were significantly blocked on pretreatment with N-acetylcysteine and overexpression of catalase.
The SFN-induced ROS generation was significantly attenuated on pretreatment with mitochondrial respiratory chain complex I inhibitors, including diphenyleneiodonium chloride and rotenone.
1(0,0,0,1) Details
7864650 Giulivi C, Boveris A, Cadenas E: Hydroxyl radical generation during mitochondrial electron transfer and the formation of 8-hydroxydesoxyguanosine in mitochondrial DNA. Arch Biochem Biophys. 1995 Feb 1;316(2):909-16.


These ESR signals were slightly increased by superoxide dismutase and abolished by catalase.
1(0,0,0,1) Details
17389326 Chen YH, Lin SJ, Lin FY, Wu TC, Tsao CR, Huang PH, Liu PL, Chen YL, Chen JW: High glucose impairs early and late endothelial progenitor cells by modifying nitric oxide-related but not oxidative stress-mediated mechanisms. Diabetes. 2007 Jun;56(6):1559-68. Epub 2007 Mar 26.


Antioxidants including vitamin C, N-acetylcysteine-and polyethylene glycol (PEG)-conjugated superoxide dismutase, and PEG-catalase had no effects, whereas pyrrolidine dithiocarbamate, diphenyleneiodonium, apocynin, and rotenone even deteriorated the downregulation of both EPCs.
0(0,0,0,0) Details
8156634 Close LA, Bowman PS, Paul RJ: Reoxygenation-induced relaxation of coronary arteries. Circ Res. 1994 May;74(5):870-81.


The reoxygenation relaxation was, however, sensitive to very low levels of oxygen and was inhibited by cyanide and rotenone, suggesting an involvement of mitochondrial metabolism.
0(0,0,0,0) Details
17349022 Saravanan KS, Sindhu KM, Mohanakumar KP: Melatonin protects against rotenone-induced oxidative stress in a hemiparkinsonian rat model. J Pineal Res. 2007 Apr;42(3):247-53.

We also studied the effect of melatonin on rotenone-induced changes in the antioxidant enzymes superoxide dismutase (SOD) and catalase in the cytosolic fractions of substantia nigra (SN), employing spectrophotometric procedures.
12(0,0,2,2) Details
11295757 Karu TI, Pyatibrat LV, Kalendo GS: Cell attachment modulation by radiation from a pulsed light diode (lambda = 820 nm) and various chemicals. Lasers Surg Med. 2001;28(3):227-36.

In parallel experiments, various chemicals (mannitol, melatonin, ethanol, ascorbic acid, superoxide dismutase, catalase, rotenone, azide, dinitrophenol (DNP), methylene blue, and hydrogen peroxide) are added to the cell suspension before or after the irradiation procedure.
7(0,0,1,2) Details
15667587 Perianayagam MC, Morena M, Jaber BL, Balakrishnan VS: Anti-oxidants reverse uraemia-induced down-regulation of mitochondrial membrane potential and interleukin-10 production. Eur J Clin Invest. 2005 Feb;35(2):148-53.

Pre-incubation with catalase and NAC restored uraemia-induced down regulation of MMP.
To assess the relative contribution of the NADPH oxidase and mitochondrial electron transport chain (ELT) to endotoxin (ET)-stimulated IL-10 production among monocytic cells, cells were incubated with and without a selective NADPH oxidase inhibitor, apocynin and mitochondrial ELT inhibitors, diphenyliodinium and rotenone, washed and ET-stimulated IL-10 production was measured.
1(0,0,0,1) 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. Biochim Biophys Acta. 1999 Jan 6;1453(1):49-62.

MPP (+)-induced pore opening and cytochrome c release were blocked by CsA, the Ca2+ uniporter inhibitor ruthenium red, the hydrophobic disulfide reagent N-ethylmaleimide, butacaine, and the free radical scavenging enzymes catalase and superoxide dismutase.
Rotenone, a classic non-competitive complex I inhibitor, completely inhibited MPP (+)-induced swelling and release of cytochrome c.
1(0,0,0,1) Details
16762927 Hidalgo C, Sanchez G, Barrientos G, Aracena-Parks P: A transverse tubule NADPH oxidase activity stimulates calcium release from isolated triads via ryanodine receptor type 1 S -glutathionylation. J Biol Chem. 2006 Sep 8;281(36):26473-82. Epub 2006 Jun 8.

NADPH or NADH elicited superoxide anion and hydrogen peroxide generation by isolated triads; both activities were inhibited by NOX inhibitors but not by rotenone.
NADH diminished the total thiol content of triads by one-third; catalase or apocynin, a NOX inhibitor, prevented this effect.
1(0,0,0,1) Details
3980458 Natarajan RD, Harding BW: Cholesterol side chain cleavage in rat adrenal supported by outer mitochondrial membrane NADH-semidehydroascorbate reductase. J Biol Chem. 1985 Apr 10;260(7):3902-5.

Rat adrenal mitochondria have an active rotenone-insensitive outer mitochondrial membrane NADH-semidehydroascorbate (NADH-SDA) reductase which supports cholesterol side chain cleavage at a rate equal to that supported by malate.
Catalase or butylated hydroxyanisole are required for the NADH-SDA reductase-supported cholesterol side chain cleavage.
1(0,0,0,1) Details
16804079 Leloup C, Magnan C, Benani A, Bonnet E, Alquier T, Offer G, Carriere A, Periquet A, Fernandez Y, Ktorza A, Casteilla L, Penicaud L: Mitochondrial reactive oxygen species are required for hypothalamic glucose sensing. Diabetes. 2006 Jul;55(7):2084-90.

Furthermore, in vivo, data demonstrate that both the glucose-induced increased neuronal activity in arcuate nucleus and the subsequent nervous-mediated insulin release might be mimicked by the mitochondrial complex blockers antimycin and rotenone, which generate mROS.
Adding antioxidants such as trolox and catalase or the uncoupler carbonyl cyanide m-chlorophenylhydrazone in order to lower mROS during glucose stimulation completely reverses both parameters.
1(0,0,0,1) Details
16647052 Muzaffar S, Shukla N, Angelini GD, Jeremy JY: Superoxide auto-augments superoxide formation and upregulates gp91 (phox) expression in porcine pulmonary artery endothelial cells: inhibition by iloprost. Eur J Pharmacol. 2006 May 24;538(1-3):108-14. Epub 2006 Mar 28.

Rotenone and allopurinol were without effect.
Pulmonary artery endothelial cells were incubated with xanthine/xanthine oxidase which generates superoxide, or tumour necrosis factor alpha (TNFalpha) or thromboxane A (2) analogue, U46619 (+/- superoxide dismutase [SOD] or catalase or iloprost) for 16 h.
1(0,0,0,1) Details
9067905 Zager RA, Burkhart K: Myoglobin toxicity in proximal human kidney cells: roles of Fe, Ca2+, H2O2, and terminal mitochondrial electron transport. Kidney Int. 1997 Mar;51(3):728-38.

Blockade of site 2 (antimycin) and site 3 (azide), but not site 1 (rotenone), mitochondrial electron transport significantly reduced myoglobin cytotoxicity.
Conversely, divergent cytochrome p450 inhibitors (cimetidine, aminobenzotriazole, troleandomycin) were without effect Catalase induced dose dependent cytoprotection, virtually complete, at a 5000 U/ml dose.
1(0,0,0,1) Details
933879 Shavlovskii GM, Fedorovich DV, Zviagil'skais RA: [A flavinogenic mutant of the yeast Pichia guilliermondii with impaired iron transport]. Mikrobiologiia. 1976 Mar-Apr;45(2):313-8.

The content of total and non-hemin iron and cytochrome c, and the activity of catalase, were lower in the cells of the mutant than in the parent cells, while the activity of riboflavin synthetase was higher.
Rotenone inhibited respiration of the intact cells of the mutant producing elevated amounts of riboflavin; therefore, flavinogenesis was not regulated by non-hemin iron on the first segment of the respiratory chain.
1(0,0,0,1) Details
7631741 Kowaltowski AJ, Castilho RF, Vercesi AE: Ca (2+)-induced mitochondrial membrane permeabilization: role of coenzyme Q redox state. Am J Physiol. 1995 Jul;269(1 Pt 1):C141-7.

Rotenone-poisoned rat liver mitochondria energized by succinate addition, after a 5-min period of preincubation in presence of 10 microM Ca2+, produce H2O2 at much faster rates, undergo extensive swelling, and are not able to retain the membrane potential and accumulated Ca2+.
The addition of either ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, ruthenium red, catalase, or dithiothreitol, just before succinate or O2 addition, prevented mitochondrial swelling, indicating the involvement of Ca2+, reactive oxygen species, and oxidation of membrane protein thiols in this process of membrane permeabilization.
1(0,0,0,1) Details
17395008 Del Carlo M, Schwartz D, Erickson EA, Loeser RF: Endogenous production of reactive oxygen species is required for stimulation of human articular chondrocyte matrix metalloproteinase production by fibronectin fragments. Free Radic Biol Med. 2007 May 1;42(9):1350-8. Epub 2007 Jan 24.

Overexpression of catalase, superoxide dismutase, or glutathione peroxidase also inhibited FN-f-stimulated MMP-13 production.
Preincubation of chondrocytes with rotenone, an inhibitor of the mitochondrial electron transport chain, or nordihydroguaiaretic acid (NDGA), a selective 5-lipoxygenase inhibitor, partially prevented FN-f-stimulated MMP-13 production and decreased MAP kinase and NF-kappaB phosphorylation.
1(0,0,0,1) Details
11710721 Sambo P, Baroni SS, Luchetti M, Paroncini P, Dusi S, Orlandini G, Gabrielli A: Oxidative stress in scleroderma: maintenance of scleroderma fibroblast phenotype by the constitutive up-regulation of reactive oxygen species generation through the NADPH oxidase complex pathway. Arthritis Rheum. 2001 Nov;44(11):2653-64.


This suppression was not seen with rotenone, a mitochondrial oxidase inhibitor, or allopurinol, a xanthine oxidase inhibitor.
0(0,0,0,0) Details
7646435 O'Donnell VB, Spycher S, Azzi A: Involvement of oxidants and oxidant-generating enzyme (s) in tumour-necrosis-factor-alpha-mediated apoptosis: role for lipoxygenase pathway but not mitochondrial respiratory chain. Biochem J. 1995 Aug 15;310 ( Pt 1):133-41.


We also demonstrated no role for mitochondrial-derived radicals/respiratory chain in the lytic pathway using specific inhibitors/uncouplers (rotenone, KCN, carboxin, fluoroacetate, antimycin, malonate, carbonyl cyanide p-trifluoromethoxyphenylhydrazone) and chloramphenicol-derived respiration-deficient cells.
0(0,0,0,0) 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. Chem Biol Interact. 2004 Dec 7;150(3):253-70.

Similarity and distinction in action of rotenone, oligomycin, N-ethylmaleimide, dithiothreitol, catalase, dibucaine, ruthenium red, cyclosporin A (CsA), and ADP on Cd2+ and/or Ca2+-induced mitochondrial dysfunction were revealed.
6(0,0,1,1) Details
6229605 Vitorica J, Machado A, Satrustegui J: Age-dependent variations in peroxide-utilizing enzymes from rat brain mitochondria and cytoplasm. J Neurochem. 1984 Feb;42(2):351-6.

On the other hand, catalase distribution parallels that of NADH-cytochrome c reductase (rotenone-insensitive), and appears to be associated with the outer membrane of brain mitochondria.
6(0,0,1,1) Details
19442964 Yin W, Li X, Feng S, Cheng W, Tang B, Shi YL, Hua ZC: Plasma membrane depolarization and Na,K-ATPase impairment induced by mitochondrial toxins augment leukemia cell apoptosis via a novel mitochondrial amplification mechanism. Biochem Pharmacol. 2009 Jul 15;78(2):191-202. Epub 2009 Apr 5.

In this study, we found mitochondrial toxin rotenone caused a rapid mitochondrial membrane potential (MMP) collapse in Jurkat cells followed by plasma membrane depolarization (PMP).
To understand the mechanisms, Jurkat cells with mtDNA depletion and catalase overexpression were used.
1(0,0,0,1) 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. Plant Cell. 2003 May;15(5):1212-26.

The cytoplasmic male-sterile mutant (CMSII) is impaired in complex I function and displays enhanced nonphosphorylating rotenone-insensitive [NAD (P) H dehydrogenases] and cyanide-insensitive (alternative oxidase) respiration.
In particular, diurnal patterns of alternative oxidase expression are lost, the relative importance of the different catalase isoforms is modified, and the transcripts, protein, and activity of cytosolic ascorbate peroxidase are enhanced markedly.
1(0,0,0,1) Details
12840017 Chen Q, Vazquez EJ, Moghaddas S, Hoppel CL, Lesnefsky EJ: Production of reactive oxygen species by mitochondria: central role of complex III. J Biol Chem. 2003 Sep 19;278(38):36027-31. Epub 2003 Jul 2.

Catalase scavenged H2O2.
Limitation of electron transport by the inhibitor rotenone immediately before ischemia decreases the production of ROS in cardiac myocytes and reduces damage to mitochondria.
1(0,0,0,1) Details
8904294 Wang JF, Jerrells TR, Spitzer JJ: Decreased production of reactive oxygen intermediates is an early event during in vitro apoptosis of rat thymocytes. Free Radic Biol Med. 1996;20(4):533-42.


In contrast to neutrophils and macrophages whose superoxide anions are released from membrane-bound NADPH oxidase, the production of ROI in thymocytes is likely to originate mainly from mitochondria, as indicated by the inhibitory effect of the addition of rotenone or antimycin A.
0(0,0,0,0) Details
18052679 Sall Diallo A, Sarr M, Mostefai HA, Carusio N, Pricci M, Andriantsitohaina R: Cognac polyphenolic compounds increase bradykinin-induced nitric oxide production in endothelial cells. Physiol Res. 2008;57(6):885-92. Epub 2007 Nov 30.


Moreover, CPC plus BK response was greater after inhibition of either NADPH oxidase by apocynin or xanthine oxidase by allopurinol but it was not affected by rotenone.
0(0,0,0,0) Details
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 ceramide-dependent inhibition of complex III followed by enforced superoxide and hydrogen peroxide formation. Exp Cell Res. 2001 Oct 15;270(1):56-65.


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 hydrogen 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 coenzyme Q to cytochrome c (1) and therefore prevents ubisemiquinone 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.
0(0,0,0,0) Details
16490285 Saravanan KS, Sindhu KM, Senthilkumar KS, Mohanakumar KP: L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats. Neurochem Int. 2006 Jul;49(1):28-40. Epub 2006 Feb 21.

The rotenone-induced elevated activities of cytosolic antioxidant enzymes superoxide dismutase and catalase showed further significant increase following L-deprenyl.
6(0,0,1,1) 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 oxygen species in dendritic cell differentiation and functions. Free Radic Biol Med. 2008 Apr 1;44(7):1443-51. Epub 2008 Jan 11.

A similar drop in ROS was observed upon addition of catalase, which caused functional effects similar to those produced by rotenone treatment.
6(0,0,1,1) 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.

Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group (P < 0.05).
6(0,0,1,1) Details
8135551 Kukielka E, Dicker E, Cederbaum AI: Increased production of reactive oxygen species by rat liver mitochondria after chronic ethanol treatment. Arch Biochem Biophys. 1994 Mar;309(2):377-86.

Mitochondrial lipid peroxidation was insensitive to superoxide dismutase, catalase, or hydroxyl radical scavengers but was sensitive to GSH and anti-oxidants such as trolox.
Modifiers of mitochondrial metabolism such as rotenone, cyanide, or an uncoupling agent, had no effect on mitochondrial production of reactive oxygen intermediates.
1(0,0,0,1) 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 selenium supplementation. Int J Biol Sci. 2007 Jul 13;3(5):335-41.


Unexpectedly, the expression of the enzymes that directly scavenge ROS decreased, including superoxide dismutases 1 and 2, glutathione peroxidase 1, and catalase.
1(0,0,0,1) Details
15598843 Han HJ, Lee YJ, Park SH, Lee JH, Taub M: High glucose-induced oxidative stress inhibits Na+/glucose cotransporter activity in renal proximal tubule cells. Am J Physiol Renal Physiol. 2005 May;288(5):F988-96. Epub 2004 Dec 14.

Pretreatment of the cultures with either 1) aminoguanidine or pyridoxamine [inhibitors of the accumulation of advanced glycation end products (AGEs)], 2) rotenone (an inhibitor of the mitochondrial electron transport chain), or 3) apocynin or diphenylene iodonium (DPI; inhibitors of NADPH oxidase) blocked the observed changes that occurred as a consequence of the incubation of the PTCs with high glucose.
Included among these changes were the observed increase in H2O2 levels, as well as an increase in lipid peroxide production, and a decrease both in the activity of catalase and in the level of glutathione (GSH), endogenous antioxidants.
1(0,0,0,1) 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. Am J Physiol Heart Circ Physiol. 2009 Jan;296(1):H226-32. Epub 2008 Nov 21.

Dihydroethidium (DHE) and dichlorodihydrofluorescein (DCF) intensities were increased by phenylephrine 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 NADPH oxidase inhibitor apocynin.
Olmesartan and TA0201, an ET type A receptor antagonist, converted vasoconstriction into vasodilation (8.5 +/- 1.2% and 10.5 +/- 0.5%, P < 0.01, respectively) in response to supernatant from phenylephrine-stimulated myocytes, which was eliminated with catalase.
1(0,0,0,1) 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. Free Radic Biol Med. 2003 Jul 1;35(1):24-32.


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.
0(0,0,0,0) 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.
0(0,0,0,0) Details
19855056 Gao Q, Zhao X, Ahmad M, Wolin MS: Mitochondrial-derived hydrogen peroxide inhibits relaxation of bovine coronary arterial smooth muscle to hypoxia through stimulation of ERK MAP kinase. Am J Physiol Heart Circ Physiol. 2009 Dec;297(6):H2262-9. Epub 2009 Oct 23.


Increasing mitochondrial superoxide with inhibitors of electron transport (10 microM rotenone and antimycin) and by opening mitochondrial ATP-dependent K+ channels with 100 microM diazoxide were observed in this study to attenuate relaxation of BCA precontracted with 30 mM KCl to hypoxia by 68-76% and 38%, respectively.
0(0,0,0,0) 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. Diabetes. 2004 May;53(5):1336-43.

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.
5(0,0,0,5) Details
10641721 Sauer H, Dagdanova A, Hescheler J, Wartenberg M: Redox-regulation of intrinsic prion expression in multicellular prostate tumor spheroids. Free Radic Biol Med. 1999 Dec;27(11-12):1276-83.

ROS generation was mediated by the mitochondrial respiratory chain and a NADPH oxidaselike enzyme, because carbonylcyanide-m-chlorophenylhydrazone (CCCP), rotenone, and diphenylene iodonium chloride (DPI) significantly reduced ROS levels.
The elevated ROS were correlated to an increased expression of PrPc, Cu/Zn superoxide dismutase (SOD-1), and catalase in small as compared with large spheroids.
2(0,0,0,2) Details
11934248 Wang HT, Yang XL, Zhang ZH, Lu JL, Xu HB: Reactive oxygen species from mitochondria mediate SW480 cells apoptosis induced by Na2SeO3. Biol Trace Elem Res. 2002 Mar;85(3):241-54.

Na2SeO3 increased the generation of intracellular ROS, whereas BAPTA-AM, rotenone, and NaCN completely inhibited the increase of ROS induced by Na2SeO3.
The intracellular ROS increase and apoptosis induced by Na2SeO3 were significantly decreased by superoxide dismutase (SOD), catalase.
1(0,0,0,1) 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. Circ Res. 2003 Sep 19;93(6):573-80. Epub 2003 Aug 14.

Diameter changes to increases in pressure gradients (20 and 100 cm H2O) were examined in the absence and the presence of rotenone (1 micromol/L), myxothiazol (100 nmol/L), cyanide (1 micromol/L), mitochondrial complex I, III, and IV inhibitors, respectively, and apocynin (3 mmol/L), a NADPH oxidase inhibitor.
Including superoxide dismutase and catalase in the perfusate reduced the ESR signals.
1(0,0,0,1) Details
202411 Thayer WS: Adriamycin stimulated superoxide formation in submitochondrial particles. Chem Biol Interact. 1977 Dec;19(3):265-78.

Rotenone-insensitive oxidation of NADH by the mitochondrial respiratory chain in the presence of oxygen caused the formation of approx 4 nmol of superoxide per min/mg of protein.
Measurements of the relative catalase activity of blood-free tissues of rabbits and rats indicated that heart contained 2 to 4% of the catalase activity of liver or kidney.
2(0,0,0,2) 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.
Overexpression of superoxide dismutase or catalase in RVLM of spontaneously hypertensive rats by gene transfer reversed mitochondrial dysfunctions and blunted the augmented O (2)(.-) and H (2) O (2) in RVLM.
2(0,0,0,2) Details
15317809 Muller FL, Liu Y, Van Remmen H: Complex III releases superoxide to both sides of the inner mitochondrial membrane. J Biol Chem. 2004 Nov 19;279(47):49064-73. Epub 2004 Aug 17.


Measurements of (mitochondrial matrix) aconitase inhibition, performed in the presence of exogenous superoxide dismutase and catalase, confirmed this hypothesis.
1(0,0,0,1) Details
15897899 Felty Q, Singh KP, Roy D: Estrogen-induced G1/S transition of G0-arrested estrogen-dependent breast cancer cells is regulated by mitochondrial oxidant signaling. Oncogene. 2005 Jul 21;24(31):4883-93.

E2-induced cell growth was reduced by antioxidants N-acetyl-L-cysteine (NAC), catalase, and the glutathione peroxidase mimic ebselen.
Flow cytometry showed that mitochondrial blockers of protein synthesis (chloramphenicol), transcription and replication (ethidium bromide), and function (rotenone, rhodamine 6G) blocked E2-induced G1 to S transition.
1(0,0,0,1) Details
12386149 Waypa GB, Marks JD, Mack MM, Boriboun C, Mungai PT, Schumacker PT: Mitochondrial reactive oxygen species trigger calcium increases during hypoxia in pulmonary arterial myocytes. Circ Res. 2002 Oct 18;91(8):719-26.

In superfused PA myocytes, diphenyleneiodonium, rotenone, and myxothiazol, which inhibit the proximal region of the ETC, attenuated hypoxia-induced calcium increases.
To test whether mitochondrial H2O2 is required to trigger [Ca2+] i increases, catalase was overexpressed in PA myocytes with the use of a recombinant adenovirus.
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7639736 Volk T, Ioannidis I, Hensel M, deGroot H, Kox WJ: Endothelial damage induced by nitric oxide: synergism with reactive oxygen species. Biochem Biophys Res Commun. 1995 Aug 4;213(1):196-203.

The toxicity of SIN-1 (5 mM), which produces both O2-. and NO., was reduced when catalase was added to remove H2O2 whereas superoxide dismutase had a marginal protective influence.
Non toxic doses of KCN (1 mM), antimycin A (1 microM), and rotenone (0.5 microM) in order to increase endogeneously produced reactive oxygen species increased toxic effects by 20-30% (p < 0.05).
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