| Name | xanthine oxidase |
|---|---|
| Synonyms | XDH; XDHA; XO; XOD; XOR; Xanthene dehydrogenase; Xanthine dehydrogenase; Xanthine dehydrogenase/oxidase… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16919899 | Lee JY, Jung GY, Heo HJ, Yun MR, Park JY, Bae SS, Hong KW, Lee WS, Kim CD: induces vascular smooth muscle cell apoptosis through mitochondrial generation of reactive species. Toxicol Lett. 2006 Oct 25;166(3):212-21. Epub 2006 Jul 15. Exposure of VSMC to HNE (1-30 microM) showed an augmented apoptotic changes in a concentration-dependent manner in association with an increased production of ROS, both of which were significantly attenuated by mitochondrial inhibitors such as rotenone (0.1 microM) and stigmatellin (0.1 microM), but not affected by other oxidase inhibitors involving oxidase, xanthine oxidase and cyclooxygenase. |
0(0,0,0,0) | Details |
| 7611477 | Pagano PJ, Ito Y, Tornheim K, Gallop PM, Tauber AI, Cohen RA: An oxidase -generating system in the rabbit aorta. . Am J Physiol. 1995 Jun;268(6 Pt 2):H2274-80. The inhibitors of xanthine oxidase, (300 microM), and of mitochondrial NADH dehydrogenase, rotenone (50 microM), had no significant effect on levels. |
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 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 oxidase by apocynin or xanthine oxidase by allopurinol but it was not affected by rotenone. |
0(0,0,0,0) | Details |
| 19729059 | Mendez-Samperio P, Perez A, Torres L: Role of reactive 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. |
0(0,0,0,0) | Details |
| 16303854 | Zhou X, Ferraris JD, Burg MB: Mitochondrial reactive species contribute to high NaCl-induced activation of the transcription factor TonEBP/OREBP. Am J Physiol Renal Physiol. 2006 May;290(5):F1169-76. Epub 2005 Nov 22. We inhibited mitochondrial ROS production in HEK293 cells with rotenone and myxothiazol, which inhibit mitochondrial complexes I and III, respectively. |
0(0,0,0,0) | Details |
| 18481258 | Wu F, Tyml K, Wilson JX: iNOS expression requires oxidase-dependent redox signaling in microvascular endothelial cells. J Cell Physiol. 2008 Oct;217(1):207-14. Unstimulated endothelial cells produced reactive species (ROS) sensitive to inhibition of oxidase (apocynin and DPI), mitochondrial respiration (rotenone) and NOS (L-NAME). |
0(0,0,0,0) | Details |
| 11415943 | Corda S, Laplace C, Vicaut E, Duranteau J: Rapid reactive species production by mitochondria in endothelial cells exposed to tumor necrosis factor-alpha is mediated by Am J Respir Cell Mol Biol. 2001 Jun;24(6):762-8. To determine the source of ROS, the mitochondrial respiratory chain inhibitors rotenone + thenoyltrifluoroacetone (TTFA), which inhibit electron entry to and antimycin A (AA), a blocker of were used. |
0(0,0,0,0) | Details |
| 10600842 | Becker LB, vanden Hoek TL, Shao ZH, Li CQ, Schumacker PT: Generation of 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). |
0(0,0,0,0) | Details |
| 16608521 | Felty Q: -induced DNA synthesis in vascular endothelial cells is mediated by ROS signaling. BMC Cardiovasc Disord. 2006 Apr 11;6:16. E2-induced ROS formation was inhibited to basal levels by cotreatment with the mitochondrial inhibitor rotenone (2 microM) and xanthine oxidase inhibitor allopurinol (50 microM). |
32(0,1,1,2) | Details |
| 9642675 | Horakova L, Stolc S, Chromikova Z, Pekarova A, Derkova L: Mechanisms of hippocampal reoxygenation injury. Mol Chem Neuropathol. 1998 Apr;33(3):223-36. The results obtained on using inhibitors of radicals generation, i.e., allopurinol, indomethacin, rotenone, and antimycin A, strongly suggest that the sources of radicals were the /xanthine oxidase system, prostaglandin synthesis, and mitochondrial respiratory chain. |
31(0,1,1,1) | Details |
| 16424801 | Lecour S, Van der Merwe E, Opie LH, Sack MN: attenuates hypoxic cell death via reactive species signaling. J Cardiovasc Pharmacol. 2006 Jan;47(1):158-63. Incubation of with cyclooxygenase-2 inhibitor, NS 398 (10 microM), or with a mitochondrial respiratory chain inhibitor, rotenone (10 microM) reduced the cytoprotective effect of in parallel with a partial diminution in ROS generation. |
0(0,0,0,0) | Details |
| 8836123 | O'Donnell VB, Azzi A: High rates of extracellular generation by cultured human fibroblasts: involvement of a lipid-metabolizing enzyme. Biochem J. 1996 Sep 15;318 ( Pt 3):805-12. Inhibitor studies showed that there was no involvement of oxidase (diphenylene iodonium, diphenyl iodonium), prostaglandin H synthase (indomethacin), xanthine oxidase (allopurinol), cytochrome P-450 or mitochondrial respiration (rotenone, antimycin A). |
0(0,0,0,0) | Details |
| 12187333 | Chen SY, Lu FJ, Gau RJ, Yang ML, Huang TS: 15-Deoxy-delta12,14- 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 m-chloro-phenylhydrazone, oligomycin, cyclosporin A and rotenone), oxidase inhibitor (diphenyleneiodonium), xanthine oxidase inhibitor (allopurinol) and NO synthase inhibitor (N-monomethyl- did not reduce the generation of ROS. |
0(0,0,0,0) | Details |
| 7529030 | Zulueta JJ, Yu FS, Hertig IA, Thannickal VJ, Hassoun PM: Release of peroxide in response to hypoxia-reoxygenation: role of an NAD (P) H oxidase-like enzyme in endothelial cell plasma membrane. Am J Respir Cell Mol Biol. 1995 Jan;12(1):41-9. Furthermore, inhibitors of cyclooxygenase (indomethacin), phospholipase A2 (quinacrine and chlorpromazine), synthase analogs), the mitochondrial electron transport chain (rotenone and and cytochrome P-450 (methoxypsoralen) had no or minimal effect on this release. |
0(0,0,0,0) | Details |
| 9115718 | Leclerc P, Gagnon C: Phosphorylation of Triton X-100 soluble and insoluble protein substrates in a demembranated/reactivated human sperm model. Mol Reprod Dev. 1996 Jun;44(2):200-11. Proteins phosphorylation during the reactivation of demembranated spermatozoa previously immobilized H2O2, + xanthine oxidase-generated reactive species, or the oxidative phosphorylation uncoupler rotenone, revealed increases in cAMP-independent phosphorylation of proteins of 16.2, 46, and 93 kDa. |
31(0,1,1,1) | 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 radicals originating from the /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. |
31(0,1,1,1) | Details |
| 15090367 | Ali MH, Pearlstein DP, Mathieu CE, Schumacker PT: Mitochondrial requirement for endothelial responses to cyclic strain: implications for mechanotransduction. Am J Physiol Lung Cell Mol Physiol. 2004 Sep;287(3):L486-96. Epub 2004 Apr 16. Mitochondrial inhibitors diphenylene iodonium or rotenone abrogated this response, whereas inhibitors of (NO) synthase (L-nitroarginine), xanthine oxidase (allopurinol), or NAD (P) H oxidase (apocynin) had no effect. |
0(0,0,0,0) | Details |
| 17762155 | Witting PK, Rayner BS, Wu BJ, Ellis NA, Stocker R: peroxide promotes endothelial dysfunction by stimulating multiple sources of radical production and decreasing 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 |
| 14642398 | Gil J, Almeida S, Oliveira CR, Rego AC: Cytosolic and mitochondrial ROS in staurosporine-induced retinal cell apoptosis. Free Radic Biol Med. 2003 Dec 1;35(11):1500-14. Endogenous sources of ROS production were investigated by testing the effect of the following inhibitors: 7-nitroindazole (7-NI), a specific inhibitor of the neuronal isoform of synthase (nNOS); arachidonyl trifluoromethyl ketone (AACOCF (3)), a phospholipase A (2) (PLA (2)) inhibitor; allopurinol, a xanthine oxidase inhibitor; and the mitochondrial inhibitors rotenone and oligomycin. |
31(0,1,1,1) | Details |
| 15941011 | Terzi A, Iraz M, Sahin S, Ilhan A, Idiz N, Fadillioglu E: Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue. Toxicol Ind Health. 2004 Sep;20(6-10):141-7. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue (P < 0.05). |
6(0,0,1,1) | Details |
| 19118162 | Basuroy S, Bhattacharya S, Leffler CW, Parfenova H: Nox4 oxidase mediates oxidative stress and apoptosis caused by TNF-alpha in cerebral vascular endothelial cells. Am J Physiol Cell Physiol. 2009 Mar;296(3):C422-32. Epub 2008 Dec 31. synthase and xanthine oxidase inhibitors (N (omega)-nitro- and allopurinol) had no effect, while mitochondrial electron transport inhibitors (CCCP, 2-thenoyltrifluoroacetone, and rotenone) attenuated TNF-alpha-induced (O (2)(*-)) and apoptosis. |
0(0,0,0,0) | 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 species generation through the 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 |
| 12210849 | Tai KK, Truong DD: Activation of -sensitive channels confers protection against rotenone-induced cell death: therapeutic implications for Parkinson's disease. J Neurosci Res. 2002 Aug 15;69(4):559-66. Pretreatment of PC12 cells with preconditioning stimuli FeSO (4) or /xanthine oxidase also confers protection against rotenone-induced cell death. |
6(0,0,1,1) | Details |
| 19371603 | O'Toole TE, Zheng YT, Hellmann J, Conklin DJ, Barski O, Bhatnagar A: Acrolein activates matrix metalloproteinases by increasing reactive species in macrophages. Toxicol Appl Pharmacol. 2009 Apr 15;236(2):194-201. Epub 2009 Feb 7. Acrolein-treatment of macrophages also led to an increase in reactive species (ROS), free intracellular ([Ca2+](i)), and xanthine oxidase (XO) activity. ROS production was prevented by allopurinol, but not by rotenone or apocynin and by buffering changes in [Ca2+](I) with BAPTA-AM. |
3(0,0,0,3) | Details |
| 17947304 | Duan Y, Gross RA, Sheu SS: Ca2+-dependent generation of mitochondrial reactive species serves as a signal for poly (ADP- polymerase-1 activation during excitotoxicity. J Physiol. 2007 Dec 15;585(Pt 3):741-58. Epub 2007 Oct 18. This ROS increase was inhibited by the mitochondrial complex inhibitors rotenone and oligomycin, but not by the cytosolic phospholipase A (2) or xanthine oxidase inhibitors. |
0(0,0,0,0) | Details |
| 11950692 | Pearlstein DP, Ali MH, Mungai PT, Hynes KL, Gewertz BL, Schumacker PT: Role of mitochondrial oxidant generation in endothelial cell responses to hypoxia. Arterioscler Thromb Vasc Biol. 2002 Apr 1;22(4):566-73. Hypoxia elicited increases in dichlorofluorescein and dihydroethidium fluorescence that were abrogated by the mitochondrial electron transport (ET) inhibitors rotenone (2 micromol/L) and diphenyleneiodonium (5 micromol/L). |
0(0,0,0,0) | Details |
| 18048066 | Robillard KR, Bone DB, Hammond JR: uptake and release by equilibrative nucleoside transporter 2 (ENT2) of rat microvascular endothelial cells. Microvasc Res. 2008 Apr;75(3):351-7. Epub 2007 Oct 18. This process involves xanthine oxidase-mediated generation of reactive species (ROS), which have been implicated in the vascular dysfunction observed in ischemia-reperfusion injury. |
3(0,0,0,3) | Details |
| 18055522 | Baudry N, Laemmel E, Vicaut E: In vivo reactive 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. By contrast, no significant inhibition was found when oxidase was inhibited by apocynin or when mitochondrial complex I or complex II was inhibited by rotenone or thenoyltrifluoroacetone. |
3(0,0,0,3) | Details |
| 16647052 | Muzaffar S, Shukla N, Angelini GD, Jeremy JY: auto-augments 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 oxidase which generates or tumour necrosis factor alpha (TNFalpha) or A (2) analogue, U46619 (+/- superoxide dismutase [SOD] or catalase or iloprost) for 16 h. |
2(0,0,0,2) | Details |
| 7532384 | Duval DL, Sieg DJ, Billings RE: Regulation of hepatic synthase by reactive intermediates and Arch Biochem Biophys. 1995 Feb 1;316(2):699-706. Hepatocytes exposed to extracellular ROI generation through a /xanthine oxidase -generating system expressed increased NOS activity and mRNA levels. NOS induction in TNF alpha-treated cells is reduced by rotenone, a mitochondrial complex 1 inhibitor. |
2(0,0,0,2) | Details |
| 18487445 | Viel EC, Benkirane K, Javeshghani D, Touyz RM, Schiffrin EL: Xanthine oxidase and mitochondria contribute to vascular generation in DOCA-salt hypertensive rats. Am J Physiol Heart Circ Physiol. 2008 Jul;295(1):H281-8. Epub 2008 May 16. O (2)(*-) generation decreased with in situ treatment by tenoyltrifluoroacetone and CCCP, inhibitors of mitochondrial electron transport complexes II and IV, respectively, whereas rotenone (mitochondrial complex I inhibitor) had no effect. |
2(0,0,0,2) | 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 DMTU, xanthine oxidase inhibition superoxide dismutase, and manipulators of expression (L-NAME, were without effect. |
1(0,0,0,1) | Details |
| 7810685 | Mohazzab KM, Wolin MS: Sites of 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 mitochondria (5 mM + 30 microM antimycin), cyclooxygenase/lipoxygenase (1 microM + 0.1 mM or autooxidation (0.1 mg/ml superoxide dismutase), resulted in the detection of minimal amounts (< 3% of of chemiluminescence. These observations were confirmed by examination of chemiluminescence produced by subcellular fractions, where the major activity detected was an oxidoreductase, which fractionated in a manner closely matching the activity of the microsomal marker enzyme rotenone-insensitive -cytochrome c reductase. |
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 species of mitochondrial origin. J Biol Chem. 2005 Oct 14;280(41):34966-73. Epub 2005 Jul 17. Exposure of mIMCD-K2 cells to exogenous O (2)(-.) generated by the /xanthine oxidase system mimicked the effect of hypertonicity on COX-2 expression and (2) release. 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 m-chlorophenylhydrazone, associated with remarkable inhibition of COX-2 expression. |
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 and antimycin A increased injury while rotenone was without significant effect on injury. |
1(0,0,0,1) | Details |
| 16413574 | Zhang C, Hein TW, Wang W, Ren Y, Shipley RD, Kuo L: Activation of JNK and xanthine oxidase by TNF-alpha impairs -mediated dilation of coronary arterioles. J Mol Cell Cardiol. 2006 Feb;40(2):247-57. Epub 2006 Jan 18. Conversely, the effects of TNF were insensitive to inhibitors of p38 (SB203580), ERK (PD98059), NAD (P) H oxidase (apocynin), or mitochondrial respiratory chain (rotenone). |
1(0,0,0,1) | Details |
| 9299367 | Vanden Hoek TL, Shao Z, Li C, Schumacker PT, Becker LB: Mitochondrial electron transport can become a significant source of oxidative injury in cardiomyocytes. J Mol Cell Cardiol. 1997 Sep;29(9):2441-50. Ischemia/reperfusion causes oxidant injury in isolated cardiomyocytes without neutrophils or xanthine oxidase. Specifically, we exposed cardiomyocytes for 1 h to the mitochondrial ETC inhibitors antimycin, and rotenone and measured oxidant generation, using the intracellular fluorescent probe 2',7'-dichlorofluorescin (DCFH, sensitive to H2O2 and |
1(0,0,0,1) | Details |
| 11766411 | Naito S, Nishimura M: Enantioselective uptake of BOF-4272, a xanthine oxidase inhibitor with a chiral sulfoxide, by isolated rat hepatocytes. Yakugaku Zasshi. 2001 Dec;121(12):989-94. Metabolic inhibitors such as antimycin, oligomycin, rotenone, carbonylcyanide m-chlorophenyl hydrazone, and carbonyl -p-(trifluromethoxy)-phenylhydrazone significantly inhibited uptake of the R (+) enantiomer, but had little effect on uptake of the S (-) enantiomer. |
1(0,0,0,1) | Details |
| 15824110 | Brown ST, Scragg JL, Boyle JP, Hudasek K, Peers C, Fearon IM: Hypoxic augmentation of Ca2+ channel currents requires a functional electron transport chain. J Biol Chem. 2005 Jun 10;280(23):21706-12. Epub 2005 Apr 11. By contrast the response to CH was absent in rho (0) cells in which the mitochondrial electron transport chain (ETC) was depleted following long term treatment with ethidium or in rho (+) cells cultured in the presence of 1 microm rotenone. CH was mimicked in rho (0) cells by the exogenous production of O2 (-.). by /xanthine oxidase. |
1(0,0,0,1) | Details |
| 16033528 | Maemura K, Zheng Q, Wada T, Ozaki M, Takao S, Aikou T, Bulkley GB, Klein AS, Sun Z: Reactive species are essential mediators in antigen presentation by Kupffer cells. Immunol Cell Biol. 2005 Aug;83(4):336-43. Scavenging of KC ROS by antioxidants, or blocking of KC ROS generation by specific inhibitors of oxidase and/or xanthine oxidase, or by specific inhibitors of the mitochondrial electron transport chain, significantly decreased OVA-specific T-cell proliferation in response to antigen presentation by KC. |
1(0,0,0,1) | Details |
| 856833 | Jarasch ED, Bruder G, Keenan TW, Franke WW: Redox constituents in milk fat globule membranes and rough endoplasmic reticulum from lactating mammary gland. J Cell Biol. 1977 Apr;73(1):223-41. Both fractions contained significant amounts of a b-type cytochrome with several properties similar to those of cytochrome b5 from liver, as well as a rotenone-insensitive - and -cytochrome c reductase. MFGM contained much more flavin and much higher activities of xanthine oxidase than the RER membranes. |
1(0,0,0,1) | Details |
| 8648915 | Zager RA: Mitochondrial free radical production induces lipid peroxidation during myohemoglobinuria. Kidney Int. 1996 Mar;49(3):741-51. This study tested the potential involvement of mitochondrial electron transport, xanthine oxidase activity, and arachidonic acid metabolism in the heme-induced peroxidative state. Site 2 (antimycin A) or site 3 hypoxia) mitochondrial respiratory chain inhibition completely blocked lipid peroxidation, whereas site 1 inhibition (rotenone) doubled its extent (presumably by shunting through NADH dehydrogenase, a free radical generating system). |
1(0,0,0,1) | Details |
| 14706836 | Talbot DA, Lambert AJ, Brand MD: Production of endogenous matrix from mitochondrial complex I leads to activation of uncoupling protein 3. FEBS Lett. 2004 Jan 2;556(1-3):111-5. generated using exogenous xanthine oxidase indirectly activates an uncoupling protein (UCP)-mediated conductance of the mitochondrial inner membrane. Both production and the GDP-sensitive conductance were suppressed by rotenone plus an antioxidant. |
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 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. We investigated the role of distinct sources of ROS, including the mitochondrial electron transport chain, NAD (P) H oxidase, xanthine oxidase, and arachidonic acid metabolism, in AGE-induced VCAM-1 expression. 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. |
1(0,0,0,1) | Details |
| 6293697 | Doroshow JH: Effect of anthracycline antibiotics on radical formation in rat heart. Cancer Res. 1983 Feb;43(2):460-72. Doxorubicin stimulated mitochondrial formation in a dose-dependent manner that also appeared to follow saturation kinetics (apparent Km of 454.55 microM); however, drug-related production by mitochondria required rather than 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. In heart cytosol, anthracycline-induced formation and consumption required and were significantly reduced by allopurinol, a potent inhibitor of xanthine oxidase (xanthine:oxygen oxidoreductase, EC 1.2.3.2). |
1(0,0,0,1) | Details |
| 12615666 | Ungvari Z, Csiszar A, Edwards JG, Kaminski PM, Wolin MS, Kaley G, Koller A: Increased production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD (P) H oxidase, and inducible synthase. Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):418-24. Epub 2003 Feb 13. METHODS AND RESULTS: The increased generation of O2*- by HHcy coronary arteries was inhibited by SOD, diphenyleneiodonium, apocynin, and apocynin plus amino but was unaffected by allopurinol and rotenone. Expression of p67phox, p22phox, and p47phox subunits and that of endothelial nitric oxide synthase, Cu,Zn-SOD, Mn-SOD, extracellular SOD (mRNA), and xanthine oxidase was unchanged. |
1(0,0,0,1) | Details |
| 6291991 | Harris EJ, Booth R, Cooper MB: The effect of generation on the ability of mitochondria to take up and retain Ca2+. FEBS Lett. 1982 Sep 20;146(2):267-72. When heart or liver mitochondria are exposed to radicals generated from + xanthine oxidase their ability to take up and to retain Ca2+ is impaired. These inhibitory effects are offset if respiration is supported by in presence of rotenone provided that a substrate is provided to maintain the reduction of |
1(0,0,0,1) | 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. Using specific inhibitors, we ruled out involvement of several oxidant-generating enzymes [cyclo-oxygenase (indomethacin), cytochrome P-450 synthase (NG-methyl- oxidase (iodonium diphenyl), xanthine oxidase (allopurinol), ribonucleotide reductase (hydroxyurea)] in TNF alpha-mediated apoptosis of the murine fibrosarcoma line, L929. We also demonstrated no role for mitochondrial-derived radicals/respiratory chain in the lytic pathway using specific inhibitors/uncouplers (rotenone, KCN, carboxin, fluoroacetate, antimycin, carbonyl p-trifluoromethoxyphenylhydrazone) and chloramphenicol-derived respiration-deficient cells. |
1(0,0,0,1) | Details |
| 9211432 | Aitken RJ, Fisher HM, Fulton N, Gomez E, Knox W, Lewis B, Irvine S: Reactive species generation by human spermatozoa is induced by exogenous and inhibited by the flavoprotein inhibitors diphenylene iodonium and quinacrine. Mol Reprod Dev. 1997 Aug;47(4):468-82. Addition of to viable populations of motile spermatozoa induced a sudden dose-dependent increase in the rate of generation via mechanisms that could not be disrupted by inhibitors of the mitochondrial electron transport chain (antimycin A, rotenone, carbonyl m-chlorophenylhydrazone [CCCP], and azide), diaphorase (dicoumarol) xanthine oxidase (allopurinol), or lactic acid dehydrogenase oxamate). |
0(0,0,0,0) | Details |
| 16531806 | Lijnen P, Papparella I, Petrov V, Semplicini A, Fagard R: Angiotensin II-stimulated collagen production in cardiac fibroblasts is mediated by reactive species. J Hypertens. 2006 Apr;24(4):757-66. Rotenone, allopurinol, indomethacin, nordihydroguiaretic acid, ketoconazole and nitro- (inhibitors of mitochondrial NAD (P) H oxidase, xanthine oxidase, cyclooxygenase, lipoxygenase, cytochrome P450 oxygenase and synthase, respectively) did not affect the angiotensin II-induced collagen production. |
0(0,0,0,0) | Details |
| 11781140 | Gonzalez A, Schmid A, Salido GM, Camello PJ, Pariente JA: XOD-catalyzed ROS generation mobilizes from intracellular stores in mouse pancreatic acinar cells. Cell Signal. 2002 Feb;14(2):153-9. In fura-2 loaded isolated mouse pancreatic acinar cells, xanthine oxidase (XOD)-catalyzed reactive species (ROS) generation caused an increase in the cytosolic Ca (2+) concentration ([Ca (2+)](i)) by release of Ca (2+) from intracellular stores. ROS still released Ca (2+) when the endoplasmic reticulum Ca (2+)-ATPase was blocked with thapsigargin (1 microM), or when rotenone (10 microM) was added to release Ca (2+) from mitochondria. |
1(0,0,0,1) | Details |
| 10967318 | Tirmenstein MA, Nicholls-Grzemski FA, Zhang JG, Fariss MW: depletion and the production of reactive species in isolated hepatocyte suspensions. Chem Biol Interact. 2000 Jul 14;127(3):201-17. In agreement with this conclusion, mitochondrial electron transport inhibitors (rotenone, thenoyltrifluoroacetone and antimycin A) increased EMS-induced lipid peroxidation and cell death, while the mitochondrial uncoupler, carbonyl m-chlorophenylhydrazone, blocked EMS- and DEM-mediated ROS production and lipid peroxidation. |
0(0,0,0,0) | Details |
| 14732287 | Herrera B, Murillo MM, Alvarez-Barrientos A, Beltran J, Fernandez M, Fabregat I: Source of early reactive species in the apoptosis induced by transforming growth factor-beta in fetal rat hepatocytes. Free Radic Biol Med. 2004 Jan 1;36(1):16-26. Rotenone, an inhibitor of the NADH dehydrogenase in mitochondrial complex I, attenuated, but did not completely inhibit, ROS-production, caspase activation, and cell death mediated by TGF-beta. |
0(0,0,0,0) | Details |
| 7814613 | Munzel T, Sayegh H, Freeman BA, Tarpey MM, Harrison DG: Evidence for enhanced vascular production in tolerance. J Clin Invest. 1995 Jan;95(1):187-94. In contrast, (1 mM) an inhibitor of xanthine oxidase, rotenone (50 microM) an inhibitor of mitochondrial electron transport and NG-nitro- (100 microM) an inhibitor of synthase did not affect the chemiluminescence signals from NTG-tolerant aortas. |
0(0,0,0,0) | 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 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 -binding superoxide dismutase, whereas inhibitors of the xanthine oxidase synthase (NG-nitro- and mitochondrial NADH dehydrogenase (rotenone) were ineffective. |
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| 19781192 | Chen Y, Zhang AH, Huang SM, Ding GX, Zhang WZ, Bao HY, Wu HM, Chen RH: oxidase-derived reactive species involved in angiotensin II-induced monocyte chemoattractant protein-1 expression in mesangial cells]. Zhonghua Bing Li Xue Za Zhi. 2009 Jul;38(7):456-61. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex Iinhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P450 oxygenase inhibitor ketoconazole and the synthase inhibitor G-nitro- methyl ester were without an effect. |
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| 17881465 | Ding G, Zhang A, Huang S, Pan X, Zhen G, Chen R, Yang T: ANG II induces c-Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR. Am J Physiol Renal Physiol. 2007 Dec;293(6):F1889-97. Epub 2007 Sep 19. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex I inhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P-450 oxygenase inhibitor ketoconazole, and the synthase inhibitor N (G)-nitro- methyl ester, were without effect. |
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