Protein Information

Name superoxide dismutase
Synonyms IPO B; Indophenoloxidase B; MNSOD; Manganese superoxide dismutase; Manganese containing superoxide dismutase; Mangano superoxide dismutase; Mn superoxide dismutase; Mn SOD…

Compound Information

Name rotenone
CAS

Reference List

PubMed Abstract RScore(About this table)
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.
6(0,0,1,1) Details
17070561 Sanchez-Reus MI, Gomez del Rio MA, Iglesias I, Elorza M, Slowing K, Benedi J: Standardized Hypericum perforatum reduces oxidative stress and increases gene expression of antioxidant enzymes on rotenone-exposed rats. Neuropharmacology. 2007 Feb;52(2):606-16. Epub 2006 Oct 27.

Rotenone treatment increased activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of malondialdehyde (MDA).
6(0,0,1,1) Details
12388366 Parinandi NL, Kleinberg MA, Usatyuk PV, Cummings RJ, Pennathur A, Cardounel AJ, Zweier JL, Garcia JG, Natarajan V: Hyperoxia-induced NAD (P) H oxidase activation and regulation by MAP kinases in human lung endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2003 Jan;284(1):L26-38. Epub 2002 Jul 26.

Exposure of HPAECs to hyperoxia for 1, 3, and 12 h increased the generation of superoxide anion, which was blocked by diphenyleneiodonium but not by rotenone or oxypurinol.
Furthermore, hyperoxia enhanced NADPH- and NADH-dependent and superoxide dismutase- or diphenyleneiodonium-inhibitable ROS production in HPAECs.
1(0,0,0,1) 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 superoxide production. J Neurosci. 2000 Aug 1;20(15):5715-23.

Treatment with a superoxide dismutase mimetic before the secondary rise conferred the same protection against cell death as a treatment before the first.
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.
1(0,0,0,1) Details
6786284 Takeshige K, Takayanagi R, Minakami S: Lipid peroxidation and the reduction of ADP-Fe3+ chelate by NADH-ubiquinone reductase preparation from bovine heart mitochondria. Biochem J. 1980 Dec 15;192(3):861-6.


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.
0(0,0,0,0) 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
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).
0(0,0,0,0) Details
19822147 Belikova NA, Glumac A, Rafikov R, Jiang J, Greenberger JS, Kagan VE, Bayir H: Radioprotection by short-term oxidative preconditioning: role of manganese superoxide dismutase. FEBS Lett. 2009 Nov 3;583(21):3437-42. Epub 2009 Oct 12.

Pre-treatment of MECs with antimycin A, rotenone or H (2) O (2) increased their survival after irradiation.
2(0,0,0,2) 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.
2(0,0,0,2) Details
19670830 Mali Y, Zisapel N: A novel decoy that interrupts G93A-superoxide dismutase gain of interaction with malate dehydrogenase improves survival in an amyotrophic lateral sclerosis cell model. J Med Chem. 2009 Sep 10;52(17):5442-8.

A cell permeable 5-carboxytetramethylrhodamine derivative of the decoy peptide improved ATP content of motor neuron derived NSC-34 cells expressing G93AhSOD1 and enhanced cell survival under rotenone and low glucose challenges.
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
15764673 Bailey SR, Mitra S, Flavahan S, Flavahan NA: Reactive oxygen species from smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries. Am J Physiol Heart Circ Physiol. 2005 Jul;289(1):H243-50. Epub 2005 Mar 11.


The inhibitor of mitochondrial complex I rotenone (10 micromol/l), the antioxidant N-acetylcysteine (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.
0(0,0,0,0) 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.
6(0,0,1,1) Details
8760145 Warner BB, Stuart L, Gebb S, Wispe JR: Redox regulation of manganese superoxide dismutase. . Am J Physiol. 1996 Jul;271(1 Pt 1):L150-8.

2(0,0,0,2) Details
179119 Loschen G, Azzi A: On the formation of hydrogen peroxide and oxygen radicals in heart mitochondria. Recent Adv Stud Cardiac Struct Metab. 1975;7:3-12.

It was shown that the component responsible for mitochondrial H2O2 formation is located between the sites of the antimycin and rotenone inhibition (Loschen et al., 1971; Boveris et al., 1972).
It was recently suggested by Rotilio et al. (1973) that enzyme systems producing H2O2 via oxygen radicals are always closely associated with a superoxide dismutase.
2(0,0,0,2) Details
12097231 Li C, Wright MM, Jackson RM: Reactive species mediated injury of human lung epithelial cells after hypoxia-reoxygenation. Exp Lung Res. 2002 Jul-Aug;28(5):373-89.

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.
Cellular manganese superoxide dismutase (MnSOD) activity (units/mg protein) decreased significantly after 24 hours of hypoxia.
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, -OH scavengers (benzoate, DMTU, mannitol), xanthine oxidase inhibition (oxypurinol), superoxide dismutase, and manipulators of nitric oxide expression (L-NAME, L-arginine) were without effect.
1(0,0,0,1) Details
2721587 Miyazaki M, Utsumi K, Sato J: Mechanisms responsible for long-term survival of adult rat hepatocytes in the presence of phenobarbital in primary culture. Exp Cell Res. 1989 Jun;182(2):415-24.

Rotenone and amobarbital, which act repressively on the PB-sensitive site in the respiratory chain and are known to inhibit the mitochondrial formation of active oxygen species with NAD-linked substances, effectively prolonged the hepatocyte survival in primary culture.
Elevation of oxygen tension in primary culture remarkably decreased the hepatocyte survival rate, which was preserved by addition of antioxidant substances, such as vitamin C, vitamin E, bifemelane, selenite, and superoxide dismutase.
1(0,0,0,1) Details
7810686 Mohazzab KM, Wolin MS: Properties of a superoxide anion-generating microsomal NADH oxidoreductase, a potential pulmonary artery PO2 sensor. Am J Physiol. 1994 Dec;267(6 Pt 1):L823-31.

Microsomes show an NADH-dependent production of superoxide anion (O2-.), as detected by lucigenin-elicited chemiluminescence, a superoxide dismutase inhibited reduction of nitro blue tetrazolium (NBT) and 2,6-dichlorophenol-indophenol, and O2 consumption.
Microsomes catalyzed an NADH-mediated reduction of several electron acceptor dyes, cytochrome c (rotenone insensitive) and methemoglobin.
1(0,0,0,1) Details
7810685 Mohazzab KM, Wolin MS: Sites of superoxide anion production detected by lucigenin in calf pulmonary artery smooth muscle. Am J Physiol. 1994 Dec;267(6 Pt 1):L815-22.

Quantitation of certain other potential sources of O2-. (under optimized conditions), including xanthine oxidase (0.1 mM hypoxanthine), mitochondria (5 mM succinate + 30 microM antimycin), cyclooxygenase/lipoxygenase (1 microM arachidonic acid + 0.1 mM NADPH), or autooxidation (0.1 mg/ml superoxide dismutase), resulted in the detection of minimal amounts (< 3% of NADH) of chemiluminescence.
These observations were confirmed by examination of chemiluminescence produced by subcellular fractions, where the major activity detected was an NADH oxidoreductase, which fractionated in a manner closely matching the activity of the microsomal marker enzyme rotenone-insensitive NADH-cytochrome c reductase.
1(0,0,0,1) Details
2457025 Nisimoto Y, Tamura M, Lambeth JD: A menadione-stimulated pyridine nucleotide oxidase from resting bovine neutrophil membranes. J Biol Chem. 1988 Aug 25;263(24):11657-63.

Cytochrome c reduction was not inhibited by several mitochondrial respiratory chain inhibitors (azide, cyanide, and rotenone) but was sensitive to thiol-reactive agents (p-chloromercuribenzoate and monoiodo acetate).
Cytochrome c reduction was stimulated 4-fold by menadione and was inhibited 70% by superoxide dismutase.
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
8380815 Sanders SP, Zweier JL, Kuppusamy P, Harrison SJ, Bassett DJ, Gabrielson EW, Sylvester JT: Hyperoxic sheep pulmonary microvascular endothelial cells generate free radicals via mitochondrial electron transport. J Clin Invest. 1993 Jan;91(1):46-52.

Superoxide dismutase (SOD) quenched both signals suggesting that the observed radicals were derived from O2-..
Blocking mitochondrial electron transport with rotenone (20 microM) markedly decreased radical generation.
1(0,0,0,1) 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
19818760 Kadota Y, Suzuki S, Ideta S, Fukinbara Y, Kawakami T, Imai H, Nakagawa Y, Sato M: Enhanced metallothionein gene expression induced by mitochondrial oxidative stress is reduced in phospholipid hydroperoxide glutathione peroxidase-overexpressed cells. Eur J Pharmacol. 2010 Jan 25;626(2-3):166-70. Epub 2009 Oct 8.


These cells were treated with respiratory inhibitors, including rotenone and 2, 4-dinitrophenol; under these conditions, the PHGPx-ov cells were more resistant to cell death than the control cells.
0(0,0,0,0) Details
17762155 Witting PK, Rayner BS, Wu BJ, Ellis NA, Stocker R: Hydrogen peroxide promotes endothelial dysfunction by stimulating multiple sources of superoxide anion radical production and decreasing nitric oxide bioavailability. Cell Physiol Biochem. 2007;20(5):255-68.


Increased cellular O (2)(-.) production was inhibited by allopurinol, diphenyliodonium and rotenone in an additive manner.
0(0,0,0,0) 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.


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.
0(0,0,0,0) Details
16107721 Behrend L, Mohr A, Dick T, Zwacka RM: Manganese superoxide dismutase induces p53-dependent senescence in colorectal cancer cells. Mol Cell Biol. 2005 Sep;25(17):7758-69.

In addition, depolarization of the mitochondrial membrane by mitochondrial inhibitors such as rotenone or antimycin A led colorectal cancer cells into p53-dependent senescence.
2(0,0,0,2) Details
8989910 Otero G, Avila MA, Emfietzoglou D, Clerch LB, Massaro D, Notario V: Increased manganese superoxide dismutase activity, protein, and mRNA levels and concurrent induction of tumor necrosis factor alpha in radiation-initiated Syrian hamster cells. Mol Carcinog. 1996 Dec;17(4):175-80.

Inhibitors of superoxide (SO) anion production (thenoyltrifluoroacetone and rotenone) decreased the concentration of Mn-SOD mRNA, raising the possibility that the generation of SO radicals participated in the upregulation of Mn-SOD in cells transformed by exposure to radiation.
2(0,0,0,2) Details
8075245 Kashkarov KP, Vasil'eva EV, Ruuge EK: [Generation of superoxide radicals by the mitochondrial respiratory chain of isolated cardiomyocytes]. Biokhimiia. 1994 Jun;59(6):813-8.

When substrates and antimycin A and/or rotenone are added, the radical production rate increased and reached its maximum in the presence of the both inhibitors.
Superoxide dismutase as well as KCN suppressed the radical production, thus being suggestive of the generation of superoxide radicals in the bc1 complex, while the mechanism of O2- production is the same as was suggested for isolated mitochondria.
1(0,0,0,1) Details
17307400 Indo HP, Davidson M, Yen HC, Suenaga S, Tomita K, Nishii T, Higuchi M, Koga Y, Ozawa T, Majima HJ: Evidence of ROS generation by mitochondria in cells with impaired electron transport chain and mitochondrial DNA damage. Mitochondrion. 2007 Feb-Apr;7(1-2):106-18. Epub 2006 Dec 13.

Furthermore, manganese superoxide dismutase (MnSOD) cDNA-transfected cells had decreased ROS.
ETC inhibitors (rotenone, 3-nitropropionic acid, thenoyltrifluoroacetone, antimycin A and sodium cyanide) were also tested to determine whether inhibitor treatment increased intracellular reactive oxygen species (ROS) generation.
1(0,0,0,1) Details
1347181 Hirai K, Ikeda K, Wang GY: Paraquat damage of rat liver mitochondria by superoxide production depends on extramitochondrial NADH. Toxicology. 1992;72(1):1-16.

These alterations were resistant to rotenone and malate plus glutamate or NADPH could not substitute for NADH.
The addition of superoxide dismutase, ferricytochrome c or p-benzoquinone protected against the breakage of mitochondria caused by paraquat plus NADH.
1(0,0,0,1) Details
9301638 Mabile L, Meilhac O, Escargueil-Blanc I, Troly M, Pieraggi MT, Salvayre R, Negre-Salvayre A: Mitochondrial function is involved in LDL oxidation mediated by human cultured endothelial cells. Arterioscler Thromb Vasc Biol. 1997 Aug;17(8):1575-82.

Inhibition of cell-mediated LDL oxidation by superoxide dismutase, EDTA, or desferrioxamine implicates a role for superoxide anion and/or transition metals in this process.
When ECs were incubated with the mitochondrial respiratory-chain inhibitors antimycin A or rotenone or with the carbonylcyanide-m-chlorophenylhydrazone uncoupler rhodamine 123, uptake and subcellular distribution were altered, and concomitantly superoxide anion production and LDL oxidation were strongly decreased.
1(0,0,0,1) 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)).
Finally, in the absence of ETCBs, overexpression of manganese containing superoxide dismutase and/or mitochondrial targeted catalase using adenoviral vectors significantly protected PC-3 cells from toxicity and oxidative stress induced by glucose deprivation with expression of both enzymes providing greater protection than was seen with either alone.
1(0,0,0,1) Details
9780311 Aten RF, Kolodecik TR, Rossi MJ, Debusscher C, Behrman HR: Prostaglandin f2alpha treatment in vivo, but not in vitro, stimulates protein kinase C-activated superoxide production by nonsteroidogenic cells of the rat corpus luteum. Biol Reprod. 1998 Nov;59(5):1069-76.

The TPA-induced response was cell number dependent and was virtually abolished by superoxide dismutase, freezing, or heating (95 degrees C for 5 min).
The response to TPA and zymosan was inhibited by the NADPH/NADH-oxidase inhibitor, diphenylene iodonium (ID50 = 5 microM for TPA), but not by the mitochondrial inhibitors, potassium cyanide, rotenone, or sodium azide.
1(0,0,0,1) 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.
1(0,0,0,1) Details
8350660 Lemeshko VV, Shekh VE: Hypotonic fragility of outer membrane and activation of external pathway of NADH oxidation in rat liver mitochondria are increased with age. Mech Ageing Dev. 1993 May;68(1-3):221-33.

Mitochondrial high amplitude swelling in a cell under some extreme conditions can possibly play a very important role in mechanisms of deterioration of energy transformation function, in activation of lipid peroxidation and mitochondrial DNA damage as a result of outer membrane disruption and release of enzymes from the intermembrane space (e.g. superoxide dismutase amd adenylate kinase).
In this work the age changes of the hypotonic fragility of the outer membrane of rat liver mitochondria and the activation of the external, rotenone-insensitive pathway of NADH oxidation have been examined.
1(0,0,0,1) Details
11045967 Kimura C, Oike M, Ito Y: Hypoxia-induced alterations in Ca (2+) mobilization in brain microvascular endothelial cells. Am J Physiol Heart Circ Physiol. 2000 Nov;279(5):H2310-8.


The impairments of Ca (2+) oscillations and CCE, but not basal [Ca (2+)](i), were restored by superoxide dismutase and the inhibitors of mitochondrial electron transport, rotenone and thenoyltrifluoroacetone (TTFA).
0(0,0,0,0) 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
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
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).
2(0,0,0,2) Details
17992568 Ahmadi FA, Grammatopoulos TN, Poczobutt AM, Jones SM, Snell LD, Das M, Zawada WM: Dopamine selectively sensitizes dopaminergic neurons to rotenone-induced apoptosis. Neurochem Res. 2008 May;33(5):886-901. Epub 2007 Nov 10.

Furthermore, mitochondrial superoxide dismutase mimetic, manganese (III) meso-tetrakis (4-benzoic acid) porphyrin, blocked activation of caspase-3, and consequent cell death.
1(0,0,0,1) 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
8882715 Takahashi T, Okamoto T, Kishi T: Characterization of NADPH-dependent ubiquinone reductase activity in rat liver cytosol: effect of various factors on ubiquinone-reducing activity and discrimination from other quinone reductases. J Biochem. 1996 Feb;119(2):256-63.


Rotenone, malonic acid, antimycin A, and KCN, which inhibit mitochondrial and microsomal electron transfer enzymes, superoxide dismutase, and acetylated cytochrome c had no effect on the NADPH-UQ reductase activity.
0(0,0,0,0) 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.
0(0,0,0,0) Details
10463952 Kiningham KK, Oberley TD, Lin S, Mattingly CA, St Clair DK: Overexpression of manganese superoxide dismutase protects against mitochondrial-initiated poly (ADP-ribose) polymerase-mediated cell death. FASEB J. 1999 Sep;13(12):1601-10.

MnSOD overexpression specifically protected against cell death upon treatment with rotenone or antimycin.
2(0,0,0,2) 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. Jpn J Cancer Res. 1992 Aug;83(8):899-906.

As for its effective sites, SOD-POE prevented a decrease in the specific activity of rotenone-sensitive NADH-ubiquinone 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.
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.


Our data on Complex III show direct extramitochondrial release of superoxide, but measurements of hydrogen peroxide production revealed that this could only account for approximately 50% of the total electron leak even in mitochondria lacking CuZn-superoxide dismutase.
2(0,0,0,2) 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
16572112 Lin CL, Wang FS, Kuo YR, Huang YT, Huang HC, Sun YC, Kuo YH: Ras modulation of superoxide activates ERK-dependent fibronectin expression in diabetes-induced renal injuries. Kidney Int. 2006 May;69(9):1593-600.

Streptozotocin-induced diabetic rats were given superoxide dismutase (SOD)-conjugated propylene glycol to scavenge superoxide.
Pretreatment with diphenyliodonium, not allopurinol or rotenone, reduced high-glucose and AGE augmentation of superoxide synthesis and fibronection expression.
1(0,0,0,1) Details
16728523 Wang JS, Lee T, Chow SE: Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men. J Appl Physiol. 2006 Sep;101(3):740-4. Epub 2006 May 25.

Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD, respectively) activities, and total and reduced-form gamma-glutamylcysteinyl glycine (t-GSH and r-GSH, respectively) contents in monocytes mediated by ox-LDL were measured.
This experiment obtained the following findings: 1) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; 2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and 3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise.
1(0,0,0,1) Details
15845907 Basta G, Lazzerini G, Del Turco S, Ratto GM, Schmidt AM, De Caterina R: At least 2 distinct pathways generating reactive oxygen species mediate vascular cell adhesion molecule-1 induction by advanced glycation end products. Arterioscler Thromb Vasc Biol. 2005 Jul;25(7):1401-7. Epub 2005 Apr 21.

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.
The inhibition of Cu/Zn superoxide dismutase inhibited both ROS and VCAM-1 induction, indicating that H2O2 by this source is involved as a mediator of VCAM-1 expression by AGEs.
1(0,0,0,1) Details
19433311 Plecita-Hlavata L, Jezek J, Jezek P: Pro-oxidant mitochondrial matrix-targeted ubiquinone MitoQ10 acts as anti-oxidant at retarded electron transport or proton pumping within Complex I. Int J Biochem Cell Biol. 2009 Aug-Sep;41(8-9):1697-707. Epub 2009 Mar 3.

To elucidate pro- and anti-oxidant action of MitoQ (10), we studied its effects on HepG2 cell respiration, mitochondrial network morphology, and rates of superoxide release (above that neutralized by superoxide dismutase) to the mitochondrial matrix (J (m)).
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.
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.
0(0,0,0,0) Details
7470494 Cherry JM, Mackellar W, Morre DJ, Crane FL, Jacobsen LB, Schirrmacher V: Evidence for a plasma membrane redox system on intact ascites tumor cells with different metastatic capacity. Biochim Biophys Acta. 1981 Jan 14;634(1):11-8.


Concurrent with these findings, neither superoxide dismutase nor rotenone affected the redox activity.
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
16790527 Aquilano K, Vigilanza P, Rotilio G, Ciriolo MR: Mitochondrial damage due to SOD1 deficiency in SH-SY5Y neuroblastoma cells: a rationale for the redundancy of SOD1. FASEB J. 2006 Aug;20(10):1683-5. Epub 2006 Jun 21.

These conditions induced a high susceptibility of SOD1-depleted cells to treatment with the mitochondrial reactive oxygen species producing agent rotenone.
Superoxide dismutases (SODs) represent the first line of defense against oxidative stress, which is considered an essential factor in several neurodegenerative diseases and aging.
2(0,0,0,2) Details
6322865 Koshkin VV: [Formation of superoxide radicals in the mitochondria of skeletal muscle] . Biokhimiia. 1983 Dec;48(12):1965-9.

The superoxide-dependent oxidation of adrenaline by skeletal muscle mitochondria (maximal inhibition by superoxide dismutase from 50 to 80%) is described.
The oxidation reaction is initiated by antimycin A but not by rotenone.
2(0,0,0,2) Details
15895284 Yamamoto N, Fukuda K, Matsushita T, Matsukawa M, Hara F, Hamanishi C: Cyclic tensile stretch stimulates the release of reactive oxygen species from osteoblast-like cells. Calcif Tissue Int. 2005 Jun;76(6):433-8. Epub 2005 May 19.

Cyclic tensile stretch also enhanced superoxide dismutase (SOD) activity.
Rotenone, an inhibitor of the mitochondrial electron transport chain, enhanced stress-induced ROS synthesis.
1(0,0,0,1) Details
6249259 Cadenas E, Boveris A, Chance B: Low-level chemiluminescence of bovine heart submitochondrial particles. Biochem J. 1980 Mar 15;186(3):659-67.

Superoxide anion seems to be involved in the chemiluminescence reactions as long as light-emission was 50-60% inhibitible by superoxide dismutase.
Antimycin and rotenone increased chemiluminescence by 50-60%; addition of substrates, NADH and succinate did not produce marked changes in the observed chemiluminescence.
1(0,0,0,1) 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 oxygen species and cause mitochondrial damage and death in motor neuron-like cells. J Neurol Sci. 2005 May 15;232(1-2):95-103.

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 glutathione by ethacrynic acid or rotenone-mediated inhibition of complex I of the mitochondrial electron transport chain.
2(0,0,0,2) Details
14663204 Sakka N, Sawada H, Izumi Y, Kume T, Katsuki H, Kaneko S, Shimohama S, Akaike A: Dopamine is involved in selectivity of dopaminergic neuronal death by rotenone. Neuroreport. 2003 Dec 19;14(18):2425-8.

The toxicity was significantly prevented by a membrane-permeable superoxide dismutase mimetic and alpha-methyl-p-tyrosine (alpha-MT), a tyrosine hydroxylase inhibitor.
1(0,0,0,1) 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. 2008 Dec 10;28(50):13511-21.

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.
Whole-brain cytochrome oxidase and superoxide dismutase activities were also increased in NIL-treated subjects in a dose-dependent manner, suggesting an in vivo transcranial effect of NIL.
1(0,0,0,1) 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
11352892 Shi Y, Patel S, Davenpeck KL, Niculescu R, Rodriguez E, Magno MG, Ormont ML, Mannion JD, Zalewski A: Oxidative stress and lipid retention in vascular grafts: comparison between venous and arterial conduits. Circulation. 2001 May 15;103(19):2408-13.


The change in oxidative stress was also reflected by lower activity of the endogenous antioxidant superoxide dismutase in SVGs than in AGs (P <0.001).
1(0,0,0,1) Details
16024921 Yang T, Zhang A, Honeggar M, Kohan DE, Mizel D, Sanders K, Hoidal JR, Briggs JP, Schnermann JB: Hypertonic induction of COX-2 in collecting duct cells by reactive oxygen species of mitochondrial origin. J Biol Chem. 2005 Oct 14;280(41):34966-73. Epub 2005 Jul 17.

The general antioxidant N-acetyl-l-cysteine (6 mM), and the superoxide dismutase mimetic TEMPO (2.0 mm) reduced COX-2 levels by 75.6 and 79.8%, respectively.
The increases in ROSs in response to hypertonic treatment were completely blocked by any one of the mitochondrial inhibitors tested, such as rotenone, thenoyltrifluoroacetone, or carbonyl cyanide m-chlorophenylhydrazone, associated with remarkable inhibition of COX-2 expression.
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
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
12657369 Waldmeier PC: Prospects for antiapoptotic drug therapy of neurodegenerative diseases. . Prog Neuropsychopharmacol Biol Psychiatry. 2003 Apr;27(2):303-21.

The issue is important for the development of antiapoptotic compounds for the treatment of this disease because of differential involvement of p53 in different mutant superoxide dismutase (SOD) mice.
These events are reasonably well reflected in some of the PD animal models, notably those involving 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone.
1(0,0,0,1) Details
18055522 Baudry N, Laemmel E, Vicaut E: In vivo reactive oxygen species production induced by ischemia in muscle arterioles of mice: involvement of xanthine oxidase and mitochondria. Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H821-8. Epub 2007 Nov 30.

This phenomenon was significantly inhibited by pretreatment with superoxide dismutase.
By contrast, no significant inhibition was found when NADPH oxidase was inhibited by apocynin or when mitochondrial complex I or complex II was inhibited by rotenone or thenoyltrifluoroacetone.
1(0,0,0,1) Details
11420302 Waypa GB, Chandel NS, Schumacker PT: Model for hypoxic pulmonary vasoconstriction involving mitochondrial oxygen sensing. Circ Res. 2001 Jun 22;88(12):1259-66.

In buffer-perfused rat lungs, rotenone, myxothiazol, and diphenyleneiodonium, which inhibit mitochondria in the proximal region of the electron transport chain (ETC), abolished HPV without attenuating the response to U46619.
To test whether reactive oxygen species (ROS) derived from mitochondria act as signaling agents in HPV, the antioxidants pyrrolidinedithiocarbamate and ebselen and the Cu,Zn superoxide dismutase inhibitor diethyldithiocarbamate were used.
1(0,0,0,1) 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. Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):2007-11. Epub 2009 Jan 27.

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).
Compared with WT, stimulation-induced increases in rhodamine-123 fluorescence were approximately 5 times larger in motor terminals from presymptomatic mice expressing mutations of human superoxide dismutase I (SOD1) that cause familial amyotrophic lateral sclerosis (SOD1-G85R, which lacks dismutase activity; SOD1-G93A, which retains dismutase activity).
1(0,0,0,1) Details
7814613 Munzel T, Sayegh H, Freeman BA, Tarpey MM, Harrison DG: Evidence for enhanced vascular superoxide anion production in nitrate tolerance. J Clin Invest. 1995 Jan;95(1):187-94.

In contrast, oxypurinol (1 mM) an inhibitor of xanthine oxidase, rotenone (50 microM) an inhibitor of mitochondrial electron transport and NG-nitro-L-arginine (100 microM) an inhibitor of nitric oxide synthase did not affect the chemiluminescence signals from NTG-tolerant aortas.
Pretreatment of tolerant aorta with liposome-entrapped, pH sensitive superoxide dismutase (600 U/ml) significantly enhanced maximal relaxation in response to NTG, SIN-1, and ACh, and effectively reduced chemiluminescence signals.
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
7678739 Hennet T, Richter C, Peterhans E: Tumour necrosis factor-alpha induces superoxide anion generation in mitochondria of L929 cells. Biochem J. 1993 Jan 15;289 ( Pt 2):587-92.

Within a few minutes after addition to L929 cells, tumour necrosis factor-alpha (TNF alpha) induced an increase in lucigenin-enhanced chemiluminescence that could be inhibited by superoxide dismutase.
The generation of superoxide anion (O2.-) was sensitive to treatment with rotenone, antimycin A and cyanide, indicating that the signal originated from mitochondria.
1(0,0,0,1) Details
14607783 Peterside IE, Selak MA, Simmons RA: Impaired oxidative phosphorylation in hepatic mitochondria in growth-retarded rats. Am J Physiol Endocrinol Metab. 2003 Dec;285(6):E1258-66.

Increased levels of manganese superoxide dismutase suggest that an antioxidant response has been mounted, and hydroxynonenal (HNE) modification of pyruvate dehydrogenase E2-(catalytic) and E3-binding protein subunits suggests that HNE-induced inactivation of this key enzyme may play a role in the mechanism of injury.
Rotenone-sensitive NADH-O2 oxidoreductase activity was similar in control and IUGR mitochondria at all ages, showing that the defect responsible for decreased pyruvate, glutamate, and alpha-ketoglutarate oxidation in IUGR liver precedes the electron transport chain and involves pyruvate and alpha-ketoglutarate dehydrogenases.
1(0,0,0,1) 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.
Superoxide dismutase addition resulted in a small diminution in light emission, but mannitol, an OH. scavenger, was without effect.
1(0,0,0,1) 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
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. PLoS One. 2009 Nov 18;4(11):e7878.

The rotenone infusion also reduced the DA content, the glutathione and superoxide dismutase activities, and induced alpha-synuclein expression, when compared to the contralateral side.
81(1,1,1,1) 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 oxygen species. J Cell Sci. 2007 Dec 1;120(Pt 23):4155-66.

Furthermore, blocking SOD2 expression by siRNA in HeLa cells increased ROS generation, autophagy and cell death induced by rotenone and TTFA.
37(0,1,2,2) Details
9893134 Heitzer T, Wenzel U, Hink U, Krollner D, Skatchkov M, Stahl RA, MacHarzina R, Brasen JH, Meinertz T, Munzel T: Increased NAD (P) H oxidase-mediated superoxide production in renovascular hypertension: evidence for an involvement of protein kinase C. Kidney Int. 1999 Jan;55(1):252-60.

Vascular O-.2 was normalized by the PKC inhibitor calphostin C, by the inhibitor of flavin-dependent oxidases, diphenylene iodonium, and recombinant heparin-binding superoxide dismutase, whereas inhibitors of the xanthine oxidase (oxypurinol), nitric oxide synthase (NG-nitro-l-arginine) and mitochondrial NADH dehydrogenase (rotenone) were ineffective.
32(0,1,1,2) Details
8146290 Gudz TI, Pandelova IG, Novgorodov SA: Stimulation of respiration in rat thymocytes induced by ionizing radiation. Radiat Res. 1994 Apr;138(1):114-20.


The radiation-induced decrease in activity of superoxide dismutase suggests free radical involvement in deleterious effects of radiation.
1(0,0,0,1) Details
19429815 Serpillon S, Floyd BC, Gupte RS, George S, Kozicky M, Neito V, Recchia F, Stanley W, Wolin MS, Gupte SA: Superoxide production by NAD (P) H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. Am J Physiol Heart Circ Physiol. 2009 Jul;297(1):H153-62. Epub 2009 May 8.

We found that myocardial G6PD activity was significantly higher in fa/fa than in lean rats, whereas superoxide dismutase and glutathione peroxidase activities were decreased (P < 0.05).
O (2)(-) levels were elevated (70-90%; P < 0.05) in the diabetic heart, and this elevation was blocked by the Nox inhibitor gp-91 (ds-tat) (50 microM) or by the mitochondrial respiratory chain inhibitors antimycin (10 microM) and rotenone (50 microM).
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
16531806 Lijnen P, Papparella I, Petrov V, Semplicini A, Fagard R: Angiotensin II-stimulated collagen production in cardiac fibroblasts is mediated by reactive oxygen species. J Hypertens. 2006 Apr;24(4):757-66.

NAD (P) H-dependent superoxide anion production was assayed as superoxide dismutase-inhibitable cytochrome c reduction.
Rotenone, allopurinol, indomethacin, nordihydroguiaretic acid, ketoconazole and nitro-L-arginine (inhibitors of mitochondrial NAD (P) H oxidase, xanthine oxidase, cyclooxygenase, lipoxygenase, cytochrome P450 oxygenase and nitric oxide synthase, respectively) did not affect the angiotensin II-induced collagen production.
1(0,0,0,1) Details
11213482 Somers MJ, Burchfield JS, Harrison DG: Evidence for a NADH/NADPH oxidase in human umbilical vein endothelial cells using electron spin resonance. Antioxid Redox Signal. 2000 Winter;2(4):779-87.

The signal was completely inhibited by either manganese superoxide dismutase (MnSOD, 100 U/ml) or the flavoprotein inhibitor diphenylene iodinium (DPI, 100 microM).
Rotenone (100 microM) did not significantly alter the signal intensity, (833 +/- 88).
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
8394271 Massa EM, Giulivi C: Alkoxyl and methyl radical formation during cleavage of tert-butyl hydroperoxide by a mitochondrial membrane-bound, redox active copper pool: an EPR study. Free Radic Biol Med. 1993 May;14(5):559-65.

Third, the enhancing effect of the respiratory chain inhibitors, antimycin A and rotenone, on free radical yield assessed in the presence of superoxide dismutase pointed to the occurrence of two potential loci in the respiratory chain involved in direct electron transfer to membrane-bound copper: one located between NADH and the rotenone-sensitive site and another, quantitatively less important, between the rotenone- and antimycin-sensitive sites.
32(0,1,1,2) Details
11342529 Yamagishi SI, Edelstein D, Du XL, Kaneda Y, Guzman M, Brownlee M: Leptin induces mitochondrial superoxide production and monocyte chemoattractant protein-1 expression in aortic endothelial cells by increasing fatty acid oxidation via protein kinase A. J Biol Chem. 2001 Jul 6;276(27):25096-100. Epub 2001 May 7.

Rotenone, thenoyltrifluoroacetone (TTFA), carbonyl cyanide m-chlorophenylhydrazone (CCCP), Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), uncoupling protein-1 (UCP1) HVJ-liposomes, or manganese superoxide dismutase (MnSOD) HVJ-liposomes completely prevented the effect of leptin, suggesting that ROS arise from mitochondrial electron transport.
31(0,1,1,1) 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
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
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.
Superoxide dismutase only slightly curtailed NBT reduction in intact cells, but inhibited it in homogenates in a concentration-dependent manner to a maximal extent of 33%.
1(0,0,0,1) Details
16990509 Moungjaroen J, Nimmannit U, Callery PS, Wang L, Azad N, Lipipun V, Chanvorachote P, Rojanasakul Y: Reactive oxygen species mediate caspase activation and apoptosis induced by lipoic acid in human lung epithelial cancer cells through Bcl-2 down-regulation. J Pharmacol Exp Ther. 2006 Dec;319(3):1062-9. Epub 2006 Sep 21.

Inhibition of ROS generation by ROS scavengers or by overexpression of antioxidant enzymes glutathione peroxidase and superoxide dismutase effectively inhibited LA-induced apoptosis, indicating the role of ROS, especially hydroperoxide and superoxide anion, in the apoptotic process.
Likewise, the mitochondrial respiratory chain inhibitor rotenone potently inhibited the apoptotic and ROS-inducing effects of LA, supporting the role of mitochondrial ROS in LA-induced cell death.
1(0,0,0,1) Details
10559793 Yang JQ, Li S, Domann FE, Buettner GR, Oberley LW: Superoxide generation in v-Ha-ras-transduced human keratinocyte HaCaT cells. Mol Carcinog. 1999 Nov;26(3):180-8.

Superoxide generation was also inhibited by diphenylene iodonium, an inhibitor of flavoproteins, including NADPH oxidase, but not by rotenone, an inhibitor of the respiratory chain of the mitochondria.
Overexpression of manganese-containing superoxide dismutase and copper and zinc-containing superoxide dismutase cDNA via adenovirus infection also attenuated superoxide generation.
1(0,0,0,1) Details
10951577 Chandel NS, Vander Heiden MG, Thompson CB, Schumacker PT: Redox regulation of p53 during hypoxia. . Oncogene. 2000 Aug 10;19(34):3840-8.

The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels.
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
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
6293697 Doroshow JH: Effect of anthracycline antibiotics on oxygen radical formation in rat heart. Cancer Res. 1983 Feb;43(2):460-72.

Doxorubicin stimulated mitochondrial superoxide formation in a dose-dependent manner that also appeared to follow saturation kinetics (apparent Km of 454.55 microM); however, drug-related superoxide production by mitochondria required NADH rather than NADPH and was significantly increased in the presence of rotenone, which suggested that the proximal portion of the mitochondrial NADH dehydrogenase complex [NADH:(acceptor) oxidoreductase, EC 1.6.99.3] was responsible for the reduction of doxorubicin at this site.
Reactive oxygen production was detected in all of our studies despite the presence of both superoxide dismutase (superoxide:superoxide oxidoreductase, EC 1.15.1.1) and glutathione peroxidase (glutathione:hydrogen peroxide oxidoreductase, EC 1.11.1.9) in each cardiac fraction.
1(0,0,0,1) Details
16337891 Li Q, Sato EF, Kira Y, Nishikawa M, Utsumi K, Inoue M: A possible cooperation of SOD1 and cytochrome c in mitochondria-dependent apoptosis. Free Radic Biol Med. 2006 Jan 1;40(1):173-81. Epub 2005 Oct 21.

We previously reported that Cu,Zn-superoxide dismutase (SOD1), a cytosolic enzyme, is also localized in mitochondria in various types of cells.
Although inhibitors of electron transport, such as rotenone, antimycin A, and KCN, also increased ROS generation, they failed to (i) oxidize the critical thiol groups in ANT, (ii) induce swelling, and (iii) release SOD1 and cytochrome c.
1(0,0,0,1) 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 oxygen species production. J Biol Chem. 2003 Mar 7;278(10):8516-25. Epub 2002 Dec 20.

The role of rotenone-induced mitochondrial ROS in apoptosis was also confirmed by the finding that HT1080 cells overexpressing magnesium superoxide dismutase were more resistant to rotenone-induced apoptosis than control cells.
6(0,0,1,1) 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. Brain Res Bull. 2006 Apr 28;69(4):465-74. Epub 2006 Mar 10.

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.
6(0,0,1,1) Details
12089069 Michelakis ED, Hampl V, Nsair A, Wu X, Harry G, Haromy A, Gurtu R, Archer SL: Diversity in mitochondrial function explains differences in vascular oxygen sensing. Circ Res. 2002 Jun 28;90(12):1307-15.

These differences relate in part to the lower expression of proximal ETC components and greater expression of mitochondrial manganese superoxide dismutase in PAs versus RAs.
The effects of hypoxia and proximal electron transport chain (pETC) inhibitors (rotenone and antimycin A) were compared in rat isolated arteries, vascular SMCs, and perfused organs.
1(0,0,0,1) Details
10783895 Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M: Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000 Apr 13;404(6779):787-90.


Here we show that this increase in reactive oxygen species is prevented by an inhibitor of electron transport chain complex II, by an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
1(0,0,0,1) 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]. Sheng Li Xue Bao. 2006 Oct 25;58(5):421-8.

Superoxide dismutase (SOD) activity was assessed with xanthine peroxidase method.
1(0,0,0,1) 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.
1(0,0,0,1) Details
20042120 Shaikh SB, Nicholson LF: Effects of chronic low dose rotenone treatment on human microglial cells. Mol Neurodegener. 2009 Dec 31;4:55.

At the end of week 4, both cell types were analysed for the presence of inclusion bodies, superoxide dismutases and cell activation (only in CHME-5 cells) using Haematoxylin and Eosin staining, immunocytochemical and western blotting methods.
1(0,0,0,1) 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
39543 Takeshige K, Minakami S: NADH- and NADPH-dependent formation of superoxide anions by bovine heart submitochondrial particles and NADH-ubiquinone reductase preparation. Biochem J. 1979 Apr 15;180(1):129-35.

The reaction was completely inhibited in the presence of superoxide dismutase, suggesting that superoxide anions (O (2) (-)) are responsible for the oxidation.
The reaction was inhibited by treatment of the preparation with p-hydroxymercuribenzoate and stimulated by treatment with rotenone.
1(0,0,0,1) Details
10600842 Becker LB, vanden Hoek TL, Shao ZH, Li CQ, Schumacker PT: Generation of superoxide in cardiomyocytes during ischemia before reperfusion. Am J Physiol. 1999 Dec;277(6 Pt 2):H2240-6.

Myxothiazol (mitochondrial site III inhibitor) attenuated oxidation to 1.3 +/- 0.1, as did the site I inhibitors rotenone (1.0 +/- 0.1), amytal (1.1 +/- 0.1), and the flavoprotein oxidase inhibitor diphenyleneiodonium (0.9 +/- 0.1).
Finally, DHE oxidation increased with Cu- and Zn-containing superoxide dismutase (SOD) inhibition using diethyldithiocarbamate (2.7 +/- 0.1) and decreased with exogenous SOD (1.1 +/- 0.1).
1(0,0,0,1) Details
9886268 Sambo P, Jannino L, Candela M, Salvi A, Donini M, Dusi S, Luchetti MM, Gabrielli A: Monocytes of patients wiht systemic sclerosis (scleroderma spontaneously release in vitro increased amounts of superoxide anion. J Invest Dermatol. 1999 Jan;112(1):78-84.

Employing the superoxide dismutase-inhibitable reduction of cytochrome c to evaluate the generation of O2*-, unmanipulated monocytes of SSc patients generated more O2*- than primary Raynaud's phenomenon patients and normal control monocytes (p = 0.0001), and the release was higher in patients with diffuse cutaneous involvement and 5 y or less disease duration (p = 0.02).
The involvement of mitochondrial oxidases was excluded by the lack of inhibition of O2*- production when monocytes were incubated in the presence of rotenone, a mitochondrial oxidase inhibitor.
1(0,0,0,1) Details
2767417 Gauduel Y, Menasche P, Duvelleroy M: Enzyme release and mitochondrial activity in reoxygenated cardiac muscle: relationship with oxygen-induced lipid peroxidation. Gen Physiol Biophys. 1989 Aug;8(4):327-40.

When an enzymatic (superoxide dismutase, 290 IU/minute) or tripeptide scavenger of oxygen radicals (reduced glutathione, 0.5 mmol/l) was administered at the end of hypoxia and during reoxygenation, the abnormal intolerance of hypoxic heart to molecular oxygen was significantly weakened; the load of lipid peroxides load, enzyme release, and vascular alteration were all reduced.
The inhibition by rotenone (100 mumol/l) of reoxidation of electron chain transfer during oxygen readmission also reduced the unfavorable cardiac accumulation of lipid peroxidation products and the release of creatine kinase.
1(0,0,0,1) Details
12390527 Wright MV, Kuhn TB: CNS neurons express two distinct plasma membrane electron transport systems implicated in neuronal viability. J Neurochem. 2002 Nov;83(3):655-64.


Reduction of both substrates was totally inhibited by epsilon-maleimidocaproic acid (MCA), a membrane-impermeant thiol reagent, and slightly inhibited by superoxide dismutase.
1(0,0,0,1) Details
12237311 St-Pierre J, Buckingham JA, Roebuck SJ, Brand MD: Topology of superoxide production from different sites in the mitochondrial electron transport chain. J Biol Chem. 2002 Nov 22;277(47):44784-90. Epub 2002 Sep 16.

However, when complex I was fully reduced using rotenone, rat mitochondria released significantly more hydrogen peroxide than pigeon mitochondria.
By measuring hydrogen peroxide production in the absence and presence of exogenous superoxide dismutase, we established the topology of superoxide production (on which side of the mitochondrial inner membrane superoxide was produced).
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.
0(0,0,0,0) 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
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.
6(0,0,1,1) 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
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
12840076 Bloomfield G, Pears C: Superoxide signalling required for multicellular development of Dictyostelium. J Cell Sci. 2003 Aug 15;116(Pt 16):3387-97. Epub 2003 Jul 2.


Scavenging superoxide, either pharmacologically or by overexpressing the enzyme superoxide dismutase, inhibits the formation of the aggregate.
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
11313892 Liu R, Li B, Qiu M: Elevated superoxide production by active H-ras enhances human lung WI-38VA-13 cell proliferation, migration and resistance to TNF-alpha. Oncogene. 2001 Mar 22;20(12):1486-96.


Upon scavenging by superoxide dismutase and other molecules that decrease the intracellular level of active H-ras mediated superoxide production, cell proliferation, migration and resistance to TNF-alpha were significantly reduced.
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.
Levels of O2- and H2O2 released from fibroblasts were estimated by the superoxide dismutase (SOD)-inhibitable cytochrome c reduction and homovanilic acid assays, respectively.
1(0,0,0,1) Details
19103678 Dedkova EN, Blatter LA: Characteristics and function of cardiac mitochondrial nitric oxide synthase. J Physiol. 2009 Feb 15;587(Pt 4):851-72. Epub 2008 Dec 22.


Collapsing the mitochondrial membrane potential with the protonophore FCCP or blocking the mitochondrial Ca (2+) uniporter with Ru360 as well as blocking the respiratory chain with rotenone or antimycin A in combination with oligomycin inhibited mitochondrial NO production.
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
15213233 Takahashi H, Tran PO, LeRoy E, Harmon JS, Tanaka Y, Robertson RP: D-Glyceraldehyde causes production of intracellular peroxide in pancreatic islets, oxidative stress, and defective beta cell function via non-mitochondrial pathways. J Biol Chem. 2004 Sep 3;279(36):37316-23. Epub 2004 Jun 22.


Neither rotenone or myxothiazol prevented D-GLYC-induced increases in islet ROS.
0(0,0,0,0) Details