| Name | aconitase |
|---|---|
| Synonyms | ACO 2; Aconitase; Citrate hydro lyase; ACO2; ACO2 protein; ACONM; Aconitase 2; Citrate hydrolyase aconitase… |
| Name | paraquat |
|---|---|
| CAS | 1,1′-dimethyl-4,4′-bipyridinium |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16139868 | Tirosh O, Pardo M, Schwartz B, Miskin R: Long-lived alphaMUPA transgenic mice show reduced SOD2 expression, enhanced apoptosis and reduced susceptibility to the carcinogen dimethylhydrazine. Mech Ageing Dev. 2005 Dec;126(12):1262-73. Epub 2005 Sep 1. Overall, alphaMUPA mice showed reduced basal levels of SOD2 gene expression and activity concomitantly with reduced lipid oxidation, increased aconitase activity and enhanced paraquat sensitivity, while maintaining the capacity to produce high levels of SOD2 in response to the inflammatory stimulus. alphaMUPA mice also showed increased resistance to DMH-induced pre-neoplasia. |
112(1,2,2,2) | Details |
| 19348901 | Cocheme HM, Murphy MP: Chapter 22 The uptake and interactions of the redox cycler paraquat with mitochondria. Methods Enzymol. 2009;456:395-417. The techniques covered include the detection and quantitation of the paraquat dication and the paraquat monocation radical (by electron paramagnetic resonance, spectrophotometry, and with an ion-selective electrode); assays for measuring paraquat-induced production by intact mitochondria or mitochondrial membranes (including aconitase inactivation, and coelenterazine chemiluminescence); methods for assessing paraquat uptake by mitochondria; and screens for identifying paraquat sensitivity or resistance in yeast mutants. |
81(1,1,1,1) | Details |
| 17013749 | Moeder W, Del Pozo O, Navarre DA, Martin GB, Klessig DF: Aconitase plays a role in regulating resistance to oxidative stress and cell death in Arabidopsis and Nicotiana benthamiana. Plant Mol Biol. 2007 Jan;63(2):273-87. Epub 2006 Oct 1. Virus-induced gene silencing (VIGS) of aconitase in Nicotiana benthamiana caused a 90% reduction in aconitase activity, stunting, spontaneous necrotic lesions, and increased resistance to paraquat. |
43(0,1,2,8) | Details |
| 19763183 | Cantu D, Schaack J, Patel M: Oxidative inactivation of mitochondrial aconitase results in iron and H2O2-mediated neurotoxicity in rat primary mesencephalic cultures. PLoS One. 2009 Sep 18;4(9):e7095. METHODOLOGY/PRINCIPAL FINDINGS: Incubation of rat primary mesencephalic cultures with the redox cycling herbicide paraquat (PQ2+) resulted in increased production of H2O2 and Fe2+ at times preceding cell death. |
7(0,0,0,7) | Details |
| 14594836 | Pomposiello PJ, Koutsolioutsou A, Carrasco D, Demple B: SoxRS-regulated expression and genetic analysis of the yggX gene of Escherichia coli. J Bacteriol. 2003 Nov;185(22):6624-32. Under exposure to paraquat, the yggX deletion strain showed a deficiency in aconitase activity compared to the isogenic wild-type strain, while expression of YggX from a multicopy plasmid increased the aconitase levels above those of the wild-type strain. |
6(0,0,1,1) | Details |
| 11814328 | Tsukamoto M, Tampo Y, Sawada M, Yonaha M: Paraquat-induced oxidative stress and dysfunction of the redox cycle in pulmonary microvascular endothelial cells. Toxicol Appl Pharmacol. 2002 Jan 15;178(2):82-92. At 4 h after exposure to paraquat at both doses, however, a marked loss in was found, together with a decrease in aconitase activity. |
6(0,0,1,1) | 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 |
| 11520895 | Li QY, Pedersen C, Day BJ, Patel M: Dependence of excitotoxic neurodegeneration on mitochondrial aconitase inactivation. J Neurochem. 2001 Aug;78(4):746-55. |
5(0,0,0,5) | Details |
| 12972424 | Missirlis F, Hu J, Kirby K, Hilliker AJ, Rouault TA, Phillips JP: Compartment-specific protection of iron- proteins by superoxide dismutase. J Biol Chem. 2003 Nov 28;278(48):47365-9. Epub 2003 Sep 12. We show that Drosophila iron regulatory protein-1 (IRP1) registers cytosolic iron and oxidative stress through its labile iron cluster by switching between cytosolic aconitase and RNA-binding functions. We also find that exposure of adults to paraquat converts cytosolic aconitase to IRP1 but has no affect on mitochondrial aconitase, indicating that paraquat generates in the cytosol but not in mitochondria. |
2(0,0,0,2) | Details |
| 15166213 | Wallace MA, Liou LL, Martins J, Clement MH, Bailey S, Longo VD, Valentine JS, Gralla EB: inhibits 4Fe-4S cluster enzymes involved in amino acid biosynthesis. J Biol Chem. 2004 Jul 30;279(31):32055-62. Epub 2004 May 27. The and biosynthetic pathways each contain a 4Fe-4S cluster enzyme homologous to aconitase and likely to be -sensitive, homoaconitase (Lys4p) and isopropylmalate dehydratase (Leu1p), respectively. |
2(0,0,0,2) | Details |
| 10224137 | Lin KI, Pasinelli P, Brown RH, Hardwick JM, Ratan RR: Decreased intracellular levels activate Sindbis virus-induced apoptosis. J Biol Chem. 1999 May 7;274(19):13650-5. Here we report that in AT-3 prostate carcinoma cells, SV infection decreases (O-2) levels within minutes of infection as monitored by an aconitase activity assay. Moreover, increasing intracellular O-2 by treatment of 3T3 cells with paraquat protects them from SV-induced death. |
1(0,0,0,1) | Details |
| 15038603 | Bradley JL, Homayoun S, Hart PE, Schapira AH, Cooper JM: Role of oxidative damage in Friedreich's ataxia. . Neurochem Res. 2004 Mar;29(3):561-7. Using fibroblasts from FRDA patients we observed that GSH levels and aconitase activities were normal, suggesting their antioxidant status was unchanged. When exposed to various agents to increase free radical generation we observed that intracellular generation induced by paraquat caused enhanced oxidative damage. |
1(0,0,0,1) | Details |
| 14720215 | Hinerfeld D, Traini MD, Weinberger RP, Cochran B, Doctrow SR, Harry J, Melov S: Endogenous mitochondrial oxidative stress: neurodegeneration, proteomic analysis, specific respiratory chain defects, and efficacious antioxidant therapy in superoxide dismutase 2 null mice. J Neurochem. 2004 Feb;88(3):657-67. Most prior studies have tested oxidative stress paradigms in mitochondria through either chemical inhibition of specific components of the respiratory chain, or adding an exogenous insult such as peroxide or paraquat to directly damage mitochondria. SOD2 null mice develop a severe neurological phenotype that includes behavioral defects, a severe spongiform encephalopathy, and a decrease in mitochondrial aconitase activity. |
1(0,0,0,1) | Details |
| 18062229 | Lee Y, Yeom J, Kang YS, Kim J, Sung JS, Jeon CO, Park W: Molecular characterization of fprB (ferredoxin- reductase) in Pseudomonas putida KT2440. J Microbiol Biotechnol. 2007 Sep;17(9):1504-12. In contrast to the fpr gene, the induction of fprB was not affected by oxidative stress agents, such as paraquat, H2O2 and t-butyl hydroperoxide. Recovery of oxidatively damaged aconitase activity was faster for the fprB mutant than for the fpr mutant, yet still slower than that for the wild type. |
1(0,0,0,1) | Details |
| 17906124 | Kang YS, Lee Y, Jung H, Jeon CO, Madsen EL, Park W: Overexpressing antioxidant enzymes enhances naphthalene biodegradation in Pseudomonas sp. strain As1. Microbiology. 2007 Oct;153(Pt 10):3246-54. All antioxidant-overexpressing recombinant strains, with the exception of one with an upregulated sodA gene due to the lac promoter [strain As1 (sodA)], exhibited resistance to the generating agent paraquat (PQ). After PQ-induced oxidative damage of the [Fe-S] enzyme aconitase, recovery of enzyme activity was enhanced in the recombinant strains. |
1(0,0,0,1) | Details |
| 16549675 | Giro M, Carrillo N, Krapp AR: Glucose-6-phosphate dehydrogenase and ferredoxin- (H) reductase contribute to damage repair during the soxRS response of Escherichia coli. Microbiology. 2006 Apr;152(Pt 4):1119-28. To evaluate whether this electron-transport system could mediate reductive repair reactions, the pathway was reconstituted in vitro from purified components; the reconstituted system was found to be functional in reactivation of oxidatively damaged iron- clusters of hydro-lyases such as aconitase and dehydratase. |
1(0,0,0,1) | Details |
| 15234109 | Orth M, Tabrizi SJ, Tomlinson C, Messmer K, Korlipara LV, Schapira AH, Cooper JM: G209A mutant alpha synuclein expression specifically enhances induced oxidative damage. Neurochem Int. 2004 Oct;45(5):669-76. We have induced G209A mutant or wild-type alpha-synuclein expression in stable HEK293 cell models to determine if this influences markers of oxidative stress and damage under normal conditions or in the presence of or paraquat. |
0(0,0,0,0) | Details |
| 16097801 | Wallace MA, Bailey S, Fukuto JM, Valentine JS, Gralla EB: Induction of phenotypes resembling CuZn-superoxide dismutase deletion in wild-type yeast cells: an in vivo assay for the role of in the toxicity of redox-cycling compounds. Chem Res Toxicol. 2005 Aug;18(8):1279-86. Such cells are exquisitely sensitive to small amounts of the herbicide paraquat (methyl viologen), which is known to produce high fluxes of in vivo via a redox-cycling mechanism. |
0(0,0,0,0) | Details |
| 19379740 | Bradley LJ, Taanman JW, Kallis C, Orrell RW: Increased sensitivity of myoblasts to oxidative stress in amyotrophic lateral sclerosis peripheral tissues. Exp Neurol. 2009 Jul;218(1):92-7. Epub 2009 Apr 18. We did, however, find an increased sensitivity to oxidative stress in myoblasts from ALS patients exposed to paraquat. |
0(0,0,0,0) | Details |
| 11098297 | Konstantinova SG, Russanov EM: Studies on paraquat-induced oxidative stress in rat liver. . Acta Physiol Pharmacol Bulg. 1999;24(4):107-11. |
0(0,0,0,0) | Details |