| Name | catalase |
|---|---|
| Synonyms | CAT; Catalase; Erythrocyte derived growth promoting factor; Carnitine O acetyltransferase; Carnitine acetylase; Carnitine acetyltransferase; CAT; Catalases… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11172004 | Liu SX, Athar M, Lippai I, Waldren C, Hei TK: Induction of oxyradicals by arsenic: implication for mechanism of genotoxicity. Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1643-8. Epub 2001 Feb 6. ESR spectroscopy with 4--2,2,6,6-tetramethyl-1-hydroxypiperidine (TEMPOL-H) as a probe in conjunction with superoxide dismutase and catalase to quench anions and peroxide, respectively, indicates that arsenite increases the levels of -driven in these cells. |
1(0,0,0,1) | Details |
| 8526746 | Lee TC, Ho IC: Modulation of cellular antioxidant defense activities by sodium arsenite in human fibroblasts. Arch Toxicol. 1995;69(7):498-504. Sodium arsenite toxicity was partly reduced by addition of catalase to the culture medium. |
81(1,1,1,1) | 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). |
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| 9288129 | Jacob AK, Hotchkiss RS, DeMeester SL, Hiramatsu M, Karl IE, Swanson PE, Cobb JP, Buchman TG: Endothelial cell apoptosis is accelerated by inorganic iron and heat via an radical dependent mechanism. Surgery. 1997 Aug;122(2):243-53; discussion 254. METHODS: HUVECs were loaded with Fe [III](ferric and ferric ammonium with 8-hydroxyquinoline as carrier and were then challenged with two stimuli of the heat shock response, authentic heat or sodium arsenite. The role of ROS was assessed with superoxide dismutase, catalase, and the reporter compound dichlorofluorescein |
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| 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 |
| 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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| 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. The decreased superoxide dismutase (SOD) activity in liver and kidney and that of catalase in liver due to arsenic treatment were also counteracted by |
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| 20028703 | Asit Kumar Bera, Rana T, Das S, Bandyopadhyay S, Bhattacharya D, Pan D, De S, Subrata Kumar Das: protects rat hepatocytes against sodium arsenite--induced cytotoxicity and oxidative damage. Hum Exp Toxicol. 2010 Feb;29(2):103-11. Epub 2009 Dec 22. Sodium arsenite-exposed hepatocytes of rat showed higher production of (NO) and increased lipid peroxidation (LPO) level vis-a-vis activity of superoxide dismutase (SOD) and catalase (CAT) were significantly lowered. |
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 |
| 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. When microsomes were incubated with various polyphenolic antioxidants, (3,4,5-trihydroxybenzoic acid) markedly increased MGST1 activity and the increase was prevented in the presence of superoxide dismutase (SOD) or catalase. 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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| 19794907 | Flora SJ, Chouhan S, Kannan GM, Mittal M, Swarnkar H: Combined administration of and monoisoamyl DMSA protects arsenic induced oxidative injury in rats. Oxid Med Cell Longev. 2008 Oct;1(1):39-45. These changes were accompanied by significant decrease in superoxide dismutase (SOD) activity and increased catalase activity. Arsenic exposed male rats (25 ppm, sodium arsenite in drinking water for 24 weeks) were treated with (100 mg/kg, i.p., once daily), monoisoamyl dimercaptosuccinic acid (MiADMSA) (50 mg/kg, oral, once daily) either individually or in combination for 5 consecutive days. |
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| 16828073 | Mittal M, Flora SJ: Effects of individual and combined exposure to sodium arsenite and on tissue oxidative stress, arsenic and levels in male mice. Chem Biol Interact. 2006 Aug 25;162(2):128-39. Epub 2006 Jun 3. An increase in the level of liver and kidney thiobarbituric acid reactive substance (TBARS) along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase, and peroxidase (GPx) and reduced GSH content were observed in both arsenic and administered mice. |
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| 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 |
| 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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| 8929554 | Watson RW, Redmond HP, Wang JH, Bouchier-Hayes D: Mechanisms involved in sodium arsenite-induced apoptosis of human neutrophils. J Leukoc Biol. 1996 Nov;60(5):625-32. To further investigate the role of oxidative injury in inducing apoptosis, the antioxidants catalase, (DMSO), (GSH), (NAC), and were investigated and we demonstrated that GSH, NAC, and were significantly protective against arsenite-induced apoptosis. |
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| 16907748 | Hrimpeng K, Prapagdee B, Banjerdkij P, Vattanaviboon P, Dubbs JM, Mongkolsuk S: Challenging Xanthomonas campestris with low levels of arsenic mediates cross-protection against oxidant killing. FEMS Microbiol Lett. 2006 Sep;262(1):121-7. Cross-protection against H (2) O (2) and organic hydroperoxide toxicity was due to increased expression of genes encoding major peroxide-metabolizing enzymes such as alkyl hydroperoxide reductase (AhpC), catalase (KatA) and organic hydroperoxide resistance protein (Ohr). |
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| 16600567 | Sun X, Li B, Li X, Wang Y, Xu Y, Jin Y, Piao F, Sun G: Effects of sodium arsenite on catalase activity, gene and protein expression in HaCaT cells. Toxicol In Vitro. 2006 Oct;20(7):1139-44. Epub 2006 Feb 28. |
12(0,0,2,2) | Details |
| 16876763 | Szymczyk KH, Kerr BA, Freeman TA, Adams CS, Steinbeck MJ: Involvement of peroxide in the differentiation and apoptosis of preosteoclastic cells exposed to arsenite. Biochem Pharmacol. 2006 Sep 14;72(6):761-9. Epub 2006 Jul 31. Long-term exposure to sodium arsenite (AsO (2)) promotes the development of various cancers. The appearance of these phenotypic markers was preceded by a low level increase in extracellular production of H (2) O (2) and was prevented by the addition of catalase (4.5microg/ml), an enzyme that removes H (2) O (2). |
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| 18183357 | Mishra D, Flora SJ: administration during chelation therapy protects arsenic-induced oxidative stress in mice. Biol Trace Elem Res. 2008 May;122(2):137-47. Epub 2008 Jan 9. Animals were chronically exposed to 25 ppm arsenite as sodium arsenite in drinking water for 12 months followed by treatment with MiADMSA (0.2 mmol/kg, orally), (0.2 mmol, orally) either alone or in combination, once daily for 5 consecutive days. Hepatic reduced catalase (CAT) and peroxidase activities showed a depletion, whereas thiobarbituric acid reactive substances (TBARS) levels increased on arsenic exposure indicating arsenite-induced oxidative stress in blood and liver. |
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| 17096945 | Sun XC, Piao FY, Wang Y, Xu YY, Li X, Li B, Jin YP, Sun GF: [Effects of sodium arsenite on catalase in human keratinocytes] . Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2006 Oct;24(10):605-7. |
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| 14567983 | Pi J, Qu W, Reece JM, Kumagai Y, Waalkes MP: Transcription factor Nrf2 activation by inorganic arsenic in cultured keratinocytes: involvement of peroxide. Exp Cell Res. 2003 Nov 1;290(2):234-45. Furthermore, when cells were pretreated with scavengers of peroxide (H (2) O (2)) such as catalase-polyethylene glycol (PEG-CAT) or Tiron, arsenic-induced nuclear Nrf2 accumulation was suppressed, whereas CuDIPSH, a cell-permeable superoxide dismutase (SOD) mimic compound that produces H (2) O (2) from (*O (2)(-)), enhanced Nrf2 nuclear accumulation. Thus, the effect of inorganic arsenic (as sodium arsenite) on Nrf2 expression and localization was studied in HaCaT cells, an immortalized human keratinocyte cell line. |
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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. Combined exposure to these toxicants produced more pronounced effects on AChE, MAO, SOD and catalase activities. |
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| 15804455 | Shila S, Kokilavani V, Subathra M, Panneerselvam C: Brain regional responses in antioxidant system to in arsenic intoxicated rat. Toxicology. 2005 May 15;210(1):25-36. Our study was designed to determine whether which has been shown to have substantial antioxidant properties, when administered (70 mg/kg body weight) once daily for 60 days along with arsenic (100 ppm sodium arsenite mixed in drinking water) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD-total SOD, Mn SOD, Cu/Zn SOD), catalase (CAT) and peroxidase (GSH-PX) in rat brain regions such as cortex, hypothalamus, striatum, cerebellum and hippocampus. |
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| 15831085 | Sinha D, Bhattacharya RK, Siddiqi M, Roy M: Amelioration of sodium arsenite-induced clastogenicity by tea extracts in Chinese hamster v79 cells. J Environ Pathol Toxicol Oncol. 2005;24(2):129-40. We also evaluated the role of tea in inducing antioxidant enzymes such as superoxide dismutase and catalase to provide protection against the oxidative stress induced by As. |
2(0,0,0,2) | Details |
| 18197836 | Sinha D, Dey S, Bhattacharya RK, Roy M: In vitro mitigation of arsenic toxicity by tea polyphenols in human lymphocytes. J Environ Pathol Toxicol Oncol. 2007;26(3):207-20. Tea also quenched the excessive production of reactive species by arsenic, reduced the elevated levels of lipid peroxidation, and increased the activity of antioxidant enzymes such as catalase, superoxide dismutase, and peroxidase. In the present study, an attempt has been made to elucidate the role of representative polyphenols and extracts of green and black tea in modulating sodium arsenite (As III)-induced DNA damage in normal human lymphocytes. |
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. On the other hand, kidney of arsenic-treated rats receiving either of the dietary protein levels showed significantly increased lipid peroxidation and decreased superoxide dismutase and catalase activities. |
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| 18619986 | Kobayashi Y, Hirano S: Effects of endogenous peroxide and on the stability of arsenic metabolites in rat bile. Toxicol Appl Pharmacol. 2008 Oct 1;232(1):33-40. Epub 2008 Jun 21. To estimate the stability of As-GSH complexes in bile, ATG or MADG was added to untreated, heat-treated, catalase-treated, or dialyzed bile, and then incubated at 37 degrees C for 10 min. |
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| 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. In liver the following biochemical changes were observed, a significant lipid peroxidation and cytochrome-P450 induction along with significant decrease in catalase and superoxide dismutase was observed at 10.5 mg/kg and 12.6 mg/kg. |
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| 11461769 | Wang TS, Hsu TY, Chung CH, Wang AS, Bau DT, Jan KY: Arsenite induces oxidative DNA adducts and DNA-protein cross-links in mammalian cells. Free Radic Biol Med. 2001 Aug 1;31(3):321-30. Arsenic is generally recognized as a nonmutagenic carcinogen because sodium arsenite induces DNA damage only at very high concentrations. We also show that catalase, and inhibitors of synthase, superoxide dismutase, and myeloperoxidase, could modulate arsenite-induced DNA damage. |
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| 17983699 | Chowdhury R, Dutta A, Chaudhuri SR, Sharma N, Giri AK, Chaudhuri K: In vitro and in vivo reduction of sodium arsenite induced toxicity by aqueous garlic extract. Food Chem Toxicol. 2008 Feb;46(2):740-51. Epub 2007 Oct 1. Moreover, AGE application in NaAsO (2) intoxicated Sprague-Dawley rats resulted in a marked inhibition of tissue lipid peroxide generation; enhanced level of total tissue sulfhydryl groups and and also increased the activities of antioxidant enzymes, superoxide dismutase and catalase to near normal. |
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| 16389662 | Gupta R, Flora SJ: Effect of Centella asiatica on arsenic induced oxidative stress and metal distribution in rats. J Appl Toxicol. 2006 May-Jun;26(3):213-22. The activities of brain superoxide dismutase (SOD) and catalase decreased marginally on arsenic exposure. |
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| 10095130 | Yih LH, Lee TC: Effects of exposure protocols on induction of kinetochore-plus and -minus micronuclei by arsenite in diploid human fibroblasts. Mutat Res. 1999 Mar 15;440(1):75-82. Catalase reduced both K+- and K--MN induced by these two exposure protocols. |
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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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| 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. |
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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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| 15689417 | Lee PC, Ho IC, Lee TC: Oxidative stress mediates sodium arsenite-induced expression of heme oxygenase-1, monocyte chemoattractant protein-1, and interleukin-6 in vascular smooth muscle cells. Toxicol Sci. 2005 May;85(1):541-50. Epub 2005 Feb 2. |
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| 16959597 | Modi M, Kaul RK, Kannan GM, Flora SJ: Co-administration of zinc and prevents arsenic-induced tissue oxidative stress in male rats. J Trace Elem Med Biol. 2006;20(3):197-204. Epub 2006 Apr 17. For 3 weeks 25 male wistar rats were exposed to arsenic as sodium arsenite (2 mg/kg, orally through gastric intubation) either alone or in combination with NAC (10 mg/kg, intraperitoneally), zinc (5 mg/kg, orally) or zinc plus NAC. Concomitant administration of zinc with arsenic showed remarkable protection against blood delta-aminolevulinic acid dehydratase (ALAD) activity as well as providing protection to hepatic biochemical variables indicative of oxidative stress (like thiobarbituric acid reactive substances (TBARS) level, catalase) and tissue injury. |
1(0,0,0,1) | Details |
| 17685460 | Bagnyukova TV, Luzhna LI, Pogribny IP, Lushchak VI: Oxidative stress and antioxidant defenses in goldfish liver in response to short-term exposure to arsenite. Environ Mol Mutagen. 2007 Oct;48(8):658-65. The present study was undertaken to investigate the effects of exposure to sodium arsenite on the pool, lipid peroxidation, protein carbonyl levels, global DNA methylation, and activities of six antioxidant enzymes in goldfish liver. Activities of the main antioxidant enzymes-superoxide dismutase, catalase, and peroxidase, were elevated after longer periods of exposure, indicating an enhanced antioxidant response. |
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| 11835394 | Hershko DD, Robb BW, Hungness ES, Luo G, Hasselgren PO: Arsenite stabilizes IkappaBalpha and prevents NF-kappaB activation in IL-1 beta-stimulated Caco-2 cells independent of the heat shock response. J Cell Biochem. 2002;84(4):687-98. Recent studies suggest that sodium arsenite downregulates NF-kappaB activity by inhibiting phosphorylation and subsequent degradation of IkappaBalpha. |
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| 7843080 | Lee TC, Ho IC: Differential cytotoxic effects of arsenic on human and animal cells. Environ Health Perspect. 1994 Sep;102 Suppl 3:101-5. Human fibroblasts (HFW) were 10-fold more susceptible than Chinese hamster ovary (CHO-K1) cells to sodium arsenite. Comparison of cellular antioxidant enzyme activities showed that CHO-K1 cells contained 3- and 8-fold more -peroxidase and catalase activities, respectively, than HFW cells. |
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| 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. Brain would be more susceptible to GR inhibition because of the decreased activities of superoxide dismutase (SOD) and catalase reported in this tissue. 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. |
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| 19111884 | Sharmila Banu G, Kumar G, Murugesan AG: Effects of leaves extract of Ocimum sanctum L. on arsenic-induced toxicity in Wistar albino rats. Food Chem Toxicol. 2009 Feb;47(2):490-5. Epub 2008 Dec 13. Activities of liver, kidney and brain superoxide dismutase and catalase also showed a decrease on arsenic exposure. |
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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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| 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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| 2050385 | Nordenson I, Beckman L: Is the genotoxic effect of arsenic mediated by free radicals? . Hum Hered. 1991;41(1):71-3. In a search for the genotoxic mechanism we have studied the effects of the -radical-scavenging enzymes superoxide dismutase (SOD) and catalase (CAT) on arsenic-induced SCEs in cultured human lymphocytes. |
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| 17188940 | Kalia K, Narula GD, Kannan GM, Flora SJ: Effects of combined administration of captopril and DMSA on arsenite induced oxidative stress and blood and tissue arsenic concentration in rats. Comp Biochem Physiol C Toxicol Pharmacol. 2007 Jan;144(4):372-9. Epub 2006 Nov 17. Animals were exposed to 100 ppm arsenite as sodium arsenite in drinking water for six weeks followed by treatment with DMSA (50 mg/kg, orally), captopril (50 mg/kg, intraperitoneally) either alone or in combination, once daily for 5 consecutive days. Kidney GSH, catalase and TBARS remained unchanged on arsenite exposure. |
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| 19631675 | Yadav RS, Sankhwar ML, Shukla RK, Chandra R, Pant AB, Islam F, Khanna VK: Attenuation of arsenic neurotoxicity by in rats. Toxicol Appl Pharmacol. 2009 Nov 1;240(3):367-76. Epub 2009 Jul 23. A significant decrease in locomotor activity, grip strength (26%) and rota-rod performance (82%) was observed in rats treated with arsenic (sodium arsenite, 20 mg/kg body weight, p.o., 28 days) as compared to controls. Increased arsenic levels in corpus striatum (6.5 fold), frontal cortex (6.3 fold) and hippocampus (7.0 fold) associated with enhanced oxidative stress in these brain regions, as evident by an increase in lipid perioxidation, protein carbonyl and a decrease in the levels of and activity of superoxide dismutase, catalase and peroxidase with differential effects were observed in arsenic treated rats compared to controls. |
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| 17613011 | Mittal M, Flora SJ: supplementation protects oxidative stress during arsenic and antagonism in male mice. Drug Chem Toxicol. 2007;30(3):263-81. Hepatic catalase activity, on the other hand, increased significantly on exposure to arsenic and |
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