| Name | aconitase |
|---|---|
| Synonyms | ACO 2; Aconitase; Citrate hydro lyase; ACO2; ACO2 protein; ACONM; Aconitase 2; Citrate hydrolyase aconitase… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12485407 | Sipos I, Tretter L, Adam-Vizi V: Quantitative relationship between inhibition of respiratory complexes and formation of reactive species in isolated nerve terminals. J Neurochem. 2003 Jan;84(1):112-8. For inhibition of complex I, III and IV, rotenone, antimycin and were used, respectively, and ROS formation was followed by measuring the activity of aconitase enzyme. |
32(0,1,1,2) | Details |
| 14674759 | Bulteau AL, Ikeda-Saito M, Szweda LI: Redox-dependent modulation of aconitase activity in intact mitochondria. . Biochemistry. 2003 Dec 23;42(50):14846-55. |
6(0,0,0,6) | Details |
| 17469137 | Crooks DR, Ghosh MC, Braun-Sommargren M, Rouault TA, Smith DR: targets m-aconitase and activates iron regulatory protein 2 in AF5 GABAergic cells. J Neurosci Res. 2007 Jun;85(8):1797-809. Using the AF5 neural-derived cell line, which displays GABAergic properties, we showed that Mn significantly increased release to 174%-214% of that of the control and that the effects of Mn exposure on the metabolism of and resembled the effects of fluorocitrate, an inhibitor of aconitase, but not the effects of other toxicants including paraquat, rotenone, or 3-nitropropionic acid. |
6(0,0,0,6) | Details |
| 11124972 | Tretter L, Adam-Vizi V: Inhibition of Krebs cycle enzymes by peroxide: A key role of [alpha]-ketoglutarate dehydrogenase in limiting production under oxidative stress. J Neurosci. 2000 Dec 15;20(24):8972-9. The enzyme that was most vulnerable to inhibition by H (2) O (2) proved to be aconitase, being completely blocked at 50 microm H (2) O (2). alpha-Ketoglutarate dehydrogenase (alpha-KGDH) was also inhibited but only at higher H (2) O (2) concentrations (>/=100 microm), and only partial inactivation was achieved. The rotenone-induced increase in [NAD (P) H] fluorescence reflecting the amount of available for the respiratory chain was also diminished by H (2) O (2), and the effect exerted at small concentrations ((BCNU), an inhibitor of glutathione reductase. |
3(0,0,0,3) | Details |
| 19526285 | Mallajosyula JK, Chinta SJ, Rajagopalan S, Nicholls DG, Andersen JK: Metabolic control analysis in a cellular model of elevated MAO-B: relevance to Parkinson's disease. Neurotox Res. 2009 Oct;16(3):186-93. Epub 2009 Mar 5. MAO-B mediated increases in H (2) O (2) also appeared to result in direct oxidative inhibition of both mitochondrial complex I and aconitase. |
2(0,0,0,2) | Details |
| 11543648 | Chen JY, Tsao GC, Zhao Q, Zheng W: Differential cytotoxicity of Mn (II) and Mn (III): special reference to mitochondrial [Fe-S] containing enzymes. Toxicol Appl Pharmacol. 2001 Sep 1;175(2):160-8. In contrast, rotenone and MPP+ did not seem to alter mtDNA levels. When mitochondrial aconitase, which possesses a [4Fe-4S] cluster, was incubated with either Mn (II) or Mn (III), both Mn species inhibited the activities of aconitase. |
2(0,0,0,2) | Details |
| 12576057 | Gostimskaya IS, Grivennikova VG, Zharova TV, Bakeeva LE, Vinogradov AD: In situ assay of the intramitochondrial enzymes: use of alamethicin for permeabilization of mitochondria. Anal Biochem. 2003 Feb 1;313(1):46-52. Alamethicin-treated mitochondria show high rotenone-sensitive oxidase, -quinone reductase, and oligomycin-sensitive and carboxyatractylate-insensitive ATPase activities. Permeabilized mitochondria quantitatively retain their aconitase and iso- dehydrogenase activities. |
1(0,0,0,1) | Details |
| 19366606 | Schwarzlander M, Fricker MD, Sweetlove LJ: Monitoring the in vivo redox state of plant mitochondria: effect of respiratory inhibitors, abiotic stress and assessment of recovery from oxidative challenge. Biochim Biophys Acta. 2009 May;1787(5):468-75. Epub 2009 Feb 3. Classical ROS-generating inhibitors of mitochondrial electron transport (rotenone, antimycin A and SHAM) had no effect on mt-roGFP oxidation when used singly, but combined inhibition of complex III and alternative oxidase by antimycin A and SHAM did cause significant oxidation. Inhibitors of complex IV and aconitase also caused oxidation of mt-roGFP2. |
1(0,0,0,1) | Details |
| 16678137 | Ho HK, Jia Y, Coe KJ, Gao Q, Doneanu CE, Hu Z, Bammler TK, Beyer RP, Fausto N, Bruschi SA, Nelson SD: Cytosolic heat shock proteins and heme oxygenase-1 are preferentially induced in response to specific and localized intramitochondrial damage by tetrafluoroethylcysteine. Biochem Pharmacol. 2006 Jun 28;72(1):80-90. Epub 2006 Mar 29. Previously, S-(1,1,2,2-tetrafluoroethyl)- (TFEC) was shown to mediate cytotoxicity by covalently modifying a well-defined group of intramitochondrial proteins including aconitase, alpha-ketoglutarate dehydrogenase (alphaKGDH) subunits, heat shock protein 60 (HSP60) and mitochondrial HSP70 (mtHSP70). Results of these studies revealed a HSP response that was significantly stronger than other well-characterized hepatotoxicants including diquat and rotenone. |
1(0,0,0,1) | Details |
| 20185797 | Ago T, Kuroda J, Pain J, Fu C, Li H, Sadoshima J: Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes. Circ Res. 2010 Feb 25. Nox4 is primarily localized in mitochondria and upregulation of Nox4 enhanced both rotenone- and diphenyleneiodonium-sensitive O2 (.-) production in mitochondria. residues in mitochondrial proteins, including aconitase and NADH dehydrogenases, were oxidized and their activities decreased in Tg-Nox4. |
1(0,0,0,1) | Details |
| 19776389 | Lustgarten MS, Jang YC, Liu Y, Muller FL, Qi W, Steinhelper M, Brooks SV, Larkin L, Shimizu T, Shirasawa T, McManus LM, Bhattacharya A, Richardson A, Van Remmen H: Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity. Am J Physiol Cell Physiol. 2009 Dec;297(6):C1520-32. Epub 2009 Sep 23. Aconitase activity was decreased by 56%, which suggests an increase in mitochondrial matrix |
1(0,0,0,1) | Details |
| 16410242 | Schonfeld P, Reiser G: Rotenone-like action of the branched-chain induces oxidative stress in mitochondria. J Biol Chem. 2006 Mar 17;281(11):7136-42. Epub 2006 Jan 12. Furthermore, inactivation of aconitase and oxidation of the mitochondrial pool show that enhanced O (2)(.) generation with chronic exposure to Phyt causes oxidative damage. |
1(0,0,0,1) | Details |
| 15317809 | Muller FL, Liu Y, Van Remmen H: Complex III releases to both sides of the inner mitochondrial membrane. J Biol Chem. 2004 Nov 19;279(47):49064-73. Epub 2004 Aug 17. Measurements of (mitochondrial matrix) aconitase inhibition, performed in the presence of exogenous superoxide dismutase and catalase, confirmed this hypothesis. |
1(0,0,0,1) | Details |
| 15569251 | Gu M, Iravani MM, Cooper JM, King D, Jenner P, Schapira AH: Pramipexole protects against apoptotic cell death by non-dopaminergic mechanisms. J Neurochem. 2004 Dec;91(5):1075-81. We have investigated the ability of pramipexole, a agonist used in the symptomatic treatment of Parkinson's disease (PD), to protect against cell death induced by 1-methyl-4-phenylpyridinium (MPP+) and rotenone in dopaminergic and non-dopaminergic cells. |
0(0,0,0,0) | Details |
| 19442717 | Schonfeld P, Dymkowska D, Wojtczak L: Acyl-CoA-induced generation of reactive species in mitochondrial preparations is due to the presence of peroxisomes. Free Radic Biol Med. 2009 Sep 1;47(5):503-9. Epub 2009 May 13. However, ROS production induced by acyl- was independent of respiration inhibition, as it was also observed in antimycin A- and rotenone-inhibited mitochondria and in submitochondrial particles in the absence of respiratory substrates (other than acyl- |
0(0,0,0,0) | Details |