| Name | glutathione S transferases |
|---|---|
| Synonyms | GST class alpha 2; Gst2; GST class alpha; GST class alpha member 2; GST gamma; GSTA 2; GSTA2; GSTA2 2… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 7568053 | Prestera T, Talalay P: Electrophile and antioxidant regulation of enzymes that detoxify carcinogens. Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8965-9. Detoxication (phase 2) enzymes, such as glutathione S-transferases (GSTs), NAD (P) H:(quinone-acceptor) oxidoreductase (QR), and UDP-glucuronsyltransferase, are induced in animal cells exposed to a variety of electrophilic compounds and phenolic antioxidants. When these three constructs were compared in Hep G2 (human) and Hepa 1c1c7 (murine) hepatoma cells, the wild-type sequence was highly activated by diverse inducers, including tert-butylhydroquinone, Michael reaction acceptors, 1,2-dithiole-3-thione, sulforaphane,2,3-dimercapto- HgCl2, sodium arsenite, and phenylarsine oxide. |
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| 8607136 | Wang Z, Dey S, Rosen BP, Rossman TG: Efflux-mediated resistance to arsenicals in arsenic-resistant and -hypersensitive Chinese hamster cells. Toxicol Appl Pharmacol. 1996 Mar;137(1):112-9. Two inhibitors of glutathione S-transferase also decreased arsenite efflux, suggesting the involvement of an arsenite- complex. |
1(0,0,0,1) | Details |
| 16433889 | Bashir S, Sharma Y, Irshad M, Gupta SD, Dogra TD: Arsenic-induced cell death in liver and brain of experimental rats. Basic Clin Pharmacol Toxicol. 2006 Jan;98(1):38-43. The activity of glutathione-S-transferase was decreased significantly in both liver and brain at 10.5 and 12.6 mg/kg. Sodium arsenite was administered orally at doses of 6.3 mg/kg, 10.5 mg/kg and 12.6 mg/kg of body weight on the basis of a lethal dose 50% (LD50) for 24 hr. |
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| 18443843 | Aggarwal M, Naraharisetti SB, Sarkar SN, Rao GS, Degen GH, Malik JK: Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study. Arch Environ Contam Toxicol. 2009 Jan;56(1):139-48. Epub 2008 Apr 29. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum and levels of (GSH) and glycosylated hemoglobin (GHb) in blood. |
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| 14971641 | Xie Y, Liu J, Liu Y, Klaassen CD, Waalkes MP: Toxicokinetic and genomic analysis of chronic arsenic exposure in multidrug-resistance mdr1a/1b (-/-) double knockout mice. Mol Cell Biochem. 2004 Jan;255(1-2):11-8. Thus, mdr1a/1b (-/-) and WT mice were exposed to sodium arsenite (0-80 ppm as arsenic) in the drinking water for 10 weeks at which time hepatic arsenic accumulation, lipid peroxidation (LPO), redox status and change in gene expression level were assessed. Arsenic induced pathological changes, elevated LPO levels and enhanced glutathione S-transferase (GST) activity, in the liver to a greater extent in mdr1a/1b (-/-) than in WT mice. |
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| 15362974 | McNeill H, Knebel A, Arthur JS, Cuenda A, Cohen P: A novel UBA and UBX domain protein that binds polyubiquitin and VCP and is a substrate for SAPKs. Biochem J. 2004 Dec 1;384(Pt 2):391-400. The amount of VCP in cell extracts that bound to immobilized GST (glutathione S-transferase)-SAKS1 was enhanced by elevating the level of polyubiquitinated proteins, while SAKS1 and VCP in extracts were coimmunoprecipitated with an antibody raised against S5a, a component of the 19 S proteasomal subunit that binds polyubiquitinated proteins. |
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| 20211736 | Chakraborty S, Ray M, Ray S: Toxicity of sodium arsenite in the gill of an economically important mollusc of India. Fish Shellfish Immunol. 2010 Mar 6. Inhibition in the activities of glutathione-s-transferase (GST) and catalase (CAT) in the species indicate impairment of its vital detoxification process and elevated oxidative stress respectively. |
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| 14691202 | Liu J, Xie Y, Ward JM, Diwan BA, Waalkes MP: Toxicogenomic analysis of aberrant gene expression in liver tumors and nontumorous livers of adult mice exposed in utero to inorganic arsenic. Toxicol Sci. 2004 Feb;77(2):249-57. Epub 2003 Dec 22. Liver tumors and nontumorous liver samples were taken at necropsy from adult male mice exposed in utero to either 42.5 or 85 ppm arsenic as sodium arsenite or unaltered water from day 8 to 18 of gestation. In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1. |
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| 11760813 | Maiti S, Chatterjee AK: Effects on levels of and some related enzymes in tissues after an acute arsenic exposure in rats and their relationship to dietary protein deficiency. Arch Toxicol. 2001 Nov;75(9):531-7. In this study, male rats of Wistar strain, maintained on either 18% or 6% protein (casein) diet, received an acute i.p. exposure to sodium arsenite (As3+) at its LD50 dose (15.86 mg/kg body weight). The glutathione-S-transferase (GST) activity significantly decreased in liver of the 18% protein-fed animals while GST increased in kidney of both the 18% and the 6% protein-fed groups. |
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| 19635623 | Flora SJ, Mittal M, Mishra D: Co-exposure to arsenic and on oxidative stress, linked enzymes, biogenic amines and DNA damage in mouse brain. J Neurol Sci. 2009 Oct 15;285(1-2):198-205. Epub 2009 Jul 26. There was also an increase in reactive species, thiobarbituric acid reactive species level, glutathione S-transferase and peroxidase activities and decreased superoxide dismutase activity, GSH:GSSG ratio, glucose 6-phosphate dehydrogenase activity. |
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| 12018983 | Sakurai T, Qu W, Sakurai MH, Waalkes MP: A major human arsenic metabolite, dimethylarsinic acid, requires to induce apoptosis. Chem Res Toxicol. 2002 May;15(5):629-37. Ethacrynic acid (EA), an inhibitor of glutathione S-transferase (GST) that catalyzes GSH-substrate conjugation, acivicin, an inhibitor of gamma-glutamyltranspeptidase (GGT) which catalyzes the initial breakdown of GSH-substrate conjugates, and aminooxyacetic acid (AOAA), an inhibitor of beta-lyase which catalyzes the final breakdown of GSH-substrate conjugates, all were effective in suppressing DMA-induced apoptosis. Thus, we studied the molecular mechanisms of in vitro cytolethality of DMA compared to that of the trivalent inorganic arsenical, sodium arsenite, using a rat liver epithelial cell line (TRL 1215). |
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| 18197399 | Manna P, Sinha M, Sil PC: Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid. Arch Toxicol. 2008 Mar;82(3):137-49. Epub 2008 Jan 16. Oral administration of NaAsO2 at a dose of 10 mg/kg body weight for 2 days caused significant accumulation of arsenic in cardiac tissues of the experimental mice in association with the reduction in cardiac antioxidant enzymes activities, namely superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and peroxidase. |
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| 1472011 | Lo JF, Wang HF, Tam MF, Lee TC: Glutathione S-transferase pi in an arsenic-resistant Chinese hamster ovary cell line. Biochem J. 1992 Dec 15;288 ( Pt 3):977-82. A glutathione S-transferase (GST) was purified from an arsenic-resistant Chinese hamster ovary cell line, SA7. Treatment with Cibacron Blue or ethacrynic acid, which are GST inhibitors, significantly decreased the resistance of SA7 cells to sodium arsenite. |
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| 12387749 | Brambila EM, Achanzar WE, Qu W, Webber MM, Waalkes MP: Chronic arsenic-exposed human prostate epithelial cells exhibit stable arsenic tolerance: mechanistic implications of altered cellular and glutathione S-transferase. Toxicol Appl Pharmacol. 2002 Sep 1;183(2):99-107. RWPE-1 cells continuously exposed to 5 microM sodium arsenite for > or =18 weeks exhibited dramatic resistance to acute arsenite toxicity. |
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| 17624716 | Sinha M, Manna P, Sil PC: a conditionally essential amino acid, ameliorates arsenic-induced cytotoxicity in murine hepatocytes. Toxicol In Vitro. 2007 Dec;21(8):1419-28. Epub 2007 Jun 2. Sodium arsenite (NaAsO (2)) was chosen as the source of arsenic. Toxin treatment caused reduction in the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR) and peroxidase (GPx). |
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| 19049818 | El-Demerdash FM, Yousef MI, Radwan FM: Ameliorating effect of on sodium arsenite-induced oxidative damage and lipid peroxidation in different rat organs. Food Chem Toxicol. 2009 Jan;47(1):249-54. Epub 2008 Nov 18. While, the activities of glutathione S-transferase, superoxide dismutase and catalase and the content of sulfhydryl groups (SH-groups) were significantly decreased in plasma and tissues compared to control. |
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| 18328521 | McNeely SC, Belshoff AC, Taylor BF, Fan TW, McCabe MJ Jr, Pinhas AR, States JC: Sensitivity to sodium arsenite in human melanoma cells depends upon susceptibility to arsenite-induced mitotic arrest. Toxicol Appl Pharmacol. 2008 Jun 1;229(2):252-61. Epub 2008 Feb 5. Inhibition of synthesis, glutathione S-transferase (GST) activity, and multidrug resistance protein (MRP) transporter function attenuated arsenite resistance, consistent with studies suggesting that arsenite is extruded from the cell as a conjugate by MRP-1. |
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| 20156518 | Das AK, Sahu R, Dua TK, Bag S, Gangopadhyay M, Sinha MK, Dewanjee S: Arsenic-induced myocardial injury: Protective role of Corchorus olitorius leaves. Food Chem Toxicol. 2010 Feb 13. The present study was undertaken to evaluate the protective effect of aqueous extract of C. olitorius leaves (AECO) against sodium arsenite (NaAsO (2)) induced cardiotoxicity in experimental rats. The animals exposed to NaAsO (2) (10mg/kg, p.o.) for 10days exhibited a significant inhibition (p <0.01) of superoxide dismutase, catalase, glutathione-S-transferase, peroxidase, glutathione reductase and level in myocardial tissues of rats. |
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| 12530527 | Yeh JY, Cheng LC, Ou BR, Whanger DP, Chang LW: Differential influences of various arsenic compounds on redox status and antioxidative enzymes in porcine endothelial cells. Cell Mol Life Sci. 2002 Nov;59(11):1972-82. The cellular response and detoxification mechanisms in porcine endothelial cells (PAECs) to arsenic trioxide (As2O3), sodium arsenite (NaAsO2) and arsenate (Na2HAsO4) were investigated. |
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| 9231701 | Wang TS, Shu YF, Liu YC, Jan KY, Huang H: peroxidase and catalase modulate the genotoxicity of arsenite. . Toxicology. 1997 Sep 5;121(3):229-37. The X-ray hypersensitive Chinese hamster ovary (CHO) cells, xrs-5, are also more sensitive to sodium arsenite in terms of cell growth and micronucleus induction than CHO-K1 cells. |
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| 8431965 | Falkner KC, McCallum GP, Cherian MG, Bend JR: Effects of acute sodium arsenite administration on the pulmonary chemical metabolizing enzymes, cytochrome P-450 monooxygenase, NAD (P) H:quinone acceptor oxidoreductase and glutathione S-transferase in guinea pig: comparison with effects in liver and kidney. Chem Biol Interact. 1993 Jan;86(1):51-68. |
81(1,1,1,1) | Details |
| 19852998 | Das AK, Bag S, Sahu R, Dua TK, Sinha MK, Gangopadhyay M, Zaman K, Dewanjee S: Protective effect of Corchorus olitorius leaves on sodium arsenite-induced toxicity in experimental rats. Food Chem Toxicol. 2010 Jan;48(1):326-35. Epub 2009 Oct 21. The animals exposed to sodium arsenite at a dose of 10mg/kg body weight p.o. for 10days exhibited a significant inhibition (p <0.01) of hepatic and renal antioxidant enzymes namely superoxide dismutase, catalase, glutathione-S-transferase, peroxidase and glutathione reductase. |
31(0,1,1,1) | Details |
| 17910617 | Manna P, Sinha M, Sil PC: Protection of arsenic-induced hepatic disorder by arjunolic acid. Basic Clin Pharmacol Toxicol. 2007 Nov;101(5):333-8. Administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly reduced the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase and peroxidase as well as depleted the level of and total thiols. |
31(0,1,1,1) | Details |
| 18273903 | Sinha M, Manna P, Sil PC: Protective effect of arjunolic acid against arsenic-induced oxidative stress in mouse brain. J Biochem Mol Toxicol. 2008 Feb;22(1):15-26. Oral administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly decreased the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and peroxidase, the level of cellular metabolites, total thiols and increased the level of |
31(0,1,1,1) | Details |
| 2732199 | Lee TC, Wei ML, Chang WJ, Ho IC, Lo JF, Jan KY, Huang H: Elevation of levels and glutathione S-transferase activity in arsenic-resistant Chinese hamster ovary cells. In Vitro Cell Dev Biol. 1989 May;25(5):442-8. The susceptibilities to sodium arsenite in parental CHO cells, revertant SA7N cells, and resistant SA7 cells were correlated with their intracellular (GSH) levels and glutathione S-transferase (GST) activity. |
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| 16256366 | Zhao Q, Chen P, Manson ME, Liu Y: Production of active recombinant mitogen-activated protein kinases through transient transfection of 293T cells. Protein Expr Purif. 2006 Apr;46(2):468-74. Epub 2005 Oct 10. We cloned JNK1, p38, and p38-regulated MAP kinase-activated protein kinase-2 into the mammalian expression vector pEBG, and expressed these protein kinases as glutathione S-transferase fusion proteins in human embryonic kidney 293T cells through transient transfection. The protein kinases were activated in vivo through treating the transfected cells with sodium arsenite and affinity-purified using -Sepharose beads. |
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| 18528686 | Naraharisetti SB, Aggarwal M, Sarkar SN, Malik JK: Concurrent subacute exposure to arsenic through drinking water and malathion via diet in male rats: effects on hepatic drug-metabolizing enzymes. Arch Toxicol. 2008 Aug;82(8):543-51. Epub 2008 Jun 5. At term, toxicity was assessed by evaluating changes in body weight, liver weight, levels of cytochrome P (450) (CYP), cytochrome b (5) and microsomal and cytosolic proteins, and activities of aminopyrine-N-demethylase (ANDM), -P-hydroxylase (APH), glutathione-S-transferase (GST) and glucuronosyltransferase (UGT) in liver. |
1(0,0,0,1) | Details |
| 10996542 | Maiti S, Chatterjee AK: Differential response of cellular antioxidant mechanism of liver and kidney to arsenic exposure and its relation to dietary protein deficiency. Environ Toxicol Pharmacol. 2000 Jun 1;8(4):227-235. The effect on antioxidant defense system of liver and kidney of sub-acute i.p. exposure to sodium arsenite (3.33 mg/kg b.w. per day) for 14 days was studied in male Wistar rats fed on an adequate (18%) or a low (6%) protein diet. Following arsenic treatment, liver showed significantly enhanced concentration of and increased activities of glutathione reductase and glutathione-S-transferase on either of the dietary protein levels. |
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| 16125204 | Shinno E, Shimoji M, Imaizumi N, Kinoshita S, Sunakawa H, Aniya Y: Activation of rat liver microsomal glutathione S-transferase by Life Sci. 2005 Nov 19;78(1):99-106. Epub 2005 Aug 25. The MGST1 activity increased by was decreased by further incubation with sodium arsenite, a sulfenic acid reducing agent, but was not with a disulfide bond reducing agent. |
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| 16386761 | Imaizumi N, Miyagi S, Aniya Y: Reactive species derived activation of rat liver microsomal glutathione S-transferase. Life Sci. 2006 May 22;78(26):2998-3006. Epub 2006 Jan 4. MGST1 activity was increased by ONOO (-) in the presence of high amounts of reducing agents including (GSH) and the activities increased by ONOO (-) or ONOO (-) plus GSH treatment were decreased by 30-40% by further incubation with (DTT, reducing disulfide) or by sodium arsenite (reducing sulfenic acid). |
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| 8097705 | Falkner KC, McCallum GP, Bend JR: Effects of arsenite treatment on NAD (P) H:quinone acceptor oxidoreductase activity in liver, lung, kidney, and heart of the rat. Drug Metab Dispos. 1993 Mar-Apr;21(2):334-7. A single dose of sodium arsenite (75 mumol/kg sc) caused a 4-fold and 2-fold increase in activity in kidney and liver, respectively, whereas beta-naphthoflavone (60 mg/kg ip once daily for 4 days) caused a 10-fold and 4.7-fold increase in kidney and liver, respectively. Arsenite also increased glutathione S-transferase [EC 2.5.1.18] activity in rat kidney. |
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