| Name | glutathione reductase |
|---|---|
| Synonyms | GLUR; GR; GRD 1; GRD1; GRase; GSR; Glutathione reductase; GRases… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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 |
| 3896786 | Pinto MC, Mata AM, Lopez-Barea J: The redox interconversion mechanism of Saccharomyces cerevisiae glutathione reductase. Eur J Biochem. 1985 Sep 2;151(2):275-81. |
4(0,0,0,4) | Details |
| 18163546 | Mishra D, Mehta A, Flora SJ: Reversal of arsenic-induced hepatic apoptosis with combined administration of DMSA and its analogues in guinea pigs: role of and linked enzymes. Chem Res Toxicol. 2008 Feb;21(2):400-7. Epub 2007 Dec 29. In the present study, we investigated (i) the role of GSH and its linked enzymes, peroxidase and glutathione reductase, in reversing chronic arsenic toxicity using a thiol chelating agent, meso-2,3-dimercaptosuccinic acid (DMSA), or one of its analogues individually or in combination; (ii) if alterations in the carbon side chain of DMSA increased efficacy; and (iii) whether the combination therapy enhance arsenic removal from hepatic tissue and prevent hepatic apoptosis. |
3(0,0,0,3) | Details |
| 15601678 | Rodriguez VM, Del Razo LM, Limon-Pacheco JH, Giordano M, Sanchez-Pena LC, Uribe-Querol E, Gutierrez-Ospina G, Gonsebatt ME: Glutathione reductase inhibition and methylated arsenic distribution in Cd1 mice brain and liver. Toxicol Sci. 2005 Mar;84(1):157-66. Epub 2004 Dec 15. To investigate whether GR inhibition could be documented in vivo, we determined the activity and levels of GR in brain as well as in liver, the main organ of arsenic metabolism in mice exposed to 2.5, 5, or 10 mg/kg/day of sodium arsenite over a period of 9 days. |
2(0,0,0,2) | Details |
| 12540038 | Ramanathan K, Balakumar BS, Panneerselvam C: Effects of and on arsenic-induced oxidative stress. Hum Exp Toxicol. 2002 Dec;21(12):675-80. Administration of and to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, and and so do the activities of superoxide dismutase, catalase, peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal. |
1(0,0,0,1) | Details |
| 15798887 | Shila S, Subathra M, Devi MA, Panneerselvam C: Arsenic intoxication-induced reduction of level and of the activity of related enzymes in rat brain regions: reversal by Arch Toxicol. 2005 Mar;79(3):140-6. Epub 2004 Nov 11. The purpose of this study was to examine the effects of DL: - (LA) on arsenic (As) induced alteration of (GSH) level and of the activity of -related enzymes- peroxidase (GSH-Px), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH)-in rat brain regions (cortex, hypothalamus, striatum, cerebellum and hippocampus). Male Wistar rats of 150+/-10 g weight were divided into four groups: control and three experimental groups supplemented with arsenic (sodium arsenite) alone (100 ppm mixed in drinking water), alone (70 mg kg (-1) body weight), arsenic plus (100 ppm arsenic in drinking water plus 70 mg kg (-1) body weight). |
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. |
2(0,0,0,2) | Details |
| 16931443 | Pal S, Chatterjee AK: Possible beneficial effects of supplementation on arsenic-induced oxidative stress in Wistar rats. Drug Chem Toxicol. 2006;29(4):423-33. Arsenic treatment (i.p. as sodium arsenite) was done at a dose of 5.55 mg/kg body weight (equivalent to 35% of LD50) per day for a period of 30 days, while supplementation (i.p.) was performed at a dose of 10 mg/kg body weight per day for the last 5 days prior to sacrifice. Arsenic-induced decreased glutathione reductase activity in liver and increased activity in kidney was appreciably counteracted by |
1(0,0,0,1) | Details |
| 12441363 | Schuliga M, Chouchane S, Snow ET: Upregulation of -related genes and enzyme activities in cultured human cells by sublethal concentrations of inorganic arsenic. Toxicol Sci. 2002 Dec;70(2):183-92. related enzymes including glutathione reductase (GR) and glutathioneS-transferase (GST) also play key roles in these processes. |
1(0,0,0,1) | Details |
| 11931390 | Prithivirajsingh S, Mishra SK, Mahadevan A: Functional analysis of a chromosomal arsenic resistance operon in Pseudomonas fluorescens strain MSP3. Mol Biol Rep. 2001;28(2):63-72. The cell free filtrates of the arsenate clones (MSA11 and MSA12) obtained from P. fluorescens containing the arsC gene showed that arsenate reduction requires glutathione reductase, (GSH), glutaredoxin and ArsC protein. We reported earlier about the detection of a chromosomally located arsenic operon (arsRBC) in a gram-negative bacterium Pseudomonas fluorescens strain MSP3, which showed resistance to elevated levels of arsenate and sodium arsenite. |
1(0,0,0,1) | Details |
| 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. |
1(0,0,0,1) | Details |
| 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). |
1(0,0,0,1) | Details |
| 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. A scavenger, diethyl (DEM), and a glutathione reductase inhibitor, carmustine, also prevented 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). |
1(0,0,0,1) | Details |
| 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. |
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. 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. |
0(0,0,0,0) | Details |
| 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. |
0(0,0,0,0) | Details |
| 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). |
0(0,0,0,0) | Details |
| 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. |
0(0,0,0,0) | 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 |