| Name | superoxide dismutase |
|---|---|
| Synonyms | IPO B; Indophenoloxidase B; MNSOD; Manganese superoxide dismutase; Manganese containing superoxide dismutase; Mangano superoxide dismutase; Mn superoxide dismutase; Mn SOD… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. NaAsO2 at 20 microM for 72 h increased Cu/Zn superoxide dismutase activity resulting in elevated intracellular peroxide levels, but As2O3 and Na2HAsO4 did not. |
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| 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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| 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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| 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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| 16600116 | Yang P, Liu QZ, Li AP, Li T, Hong X, Zhou JW: [The relationship between hormesis of proliferation and oxidative stress induced by sodium arsenite in human embryo lung fibroblasts]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2006 Feb;24(2):103-5. The cell proliferation, the reactive species (ROS) level, the malondialdehyde (MDA) content and the activity of peroxide (GSH-Px) and the superoxide dismutase (SOD) in HELF were detected respectively. |
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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. |
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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. |
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| 20144955 | Chandronitha C, Ananthi S, Ramakrishnan G, Lakshmisundaram R, Gayathri V, Vasanthi HR: Protective role of -rich fraction of Camellia sinensis in tissue arsenic burden in Sprague Dawley rats. Hum Exp Toxicol. 2010 Feb 9. Administration of sodium arsenite (100 mg/kg/day) for 28 days in Sprague Dawley female rats resulted in significant reduction of biochemical parameters such as delta-aminolevulinic acid dehydratase (ALAD), (GSH), peroxidase (GPx), superoxide dismutase (SOD) and elevation of thiobarbituric acid reactive substances (TBARS) and the index of / (NOx) levels. |
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| 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. |
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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 |
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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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| 17479414 | Yang P, He XQ, Peng L, Li AP, Wang XR, Zhou JW, Liu QZ: The role of oxidative stress in hormesis induced by sodium arsenite in human embryo lung fibroblast (HELF) cellular proliferation model. J Toxicol Environ Health A. 2007 Jun;70(11):976-83. To investigate the role of oxidative stress in hormetic phenomena associated with cell proliferation induced by sodium arsenite, the levels of reactive species (ROS), lipid peroxidation (LPO), and heat-shock proteins (HSP) and the activities of peroxidase (GSH-Px) and superoxide dismutase (SOD) were measured in human embryo lung fibroblast (HELF) cells after treatment with sodium arsenite at various concentrations for differing times. |
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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. |
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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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| 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. Lipid peroxidation and superoxide dismutase activity of liver remained unaltered on either of the dietary protein levels. |
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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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| 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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| 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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| 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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| 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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| 8526746 | Lee TC, Ho IC: Modulation of cellular antioxidant defense activities by sodium arsenite in human fibroblasts. Arch Toxicol. 1995;69(7):498-504. |
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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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| 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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| 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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| 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. |
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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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| 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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| 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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| 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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| 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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| 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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| 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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| 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 also decreased Cu/Zn superoxide dismutase activity in both mdr1a/1b (-/-) and WT mice. |
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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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| 2847725 | Kapoor M, Sveenivasan GM: The heat shock response of Neurospora crassa: stress-induced thermotolerance in relation to peroxidase and superoxide dismutase levels. Biochem Biophys Res Commun. 1988 Nov 15;156(3):1097-102. Heat shock and other treatments, including cadmium peroxide and sodium arsenite, led to the induction of high levels of peroxidase activity as well as thermotolerance in Neurospora crassa. |
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| 15964037 | Requejo R, Tena M: Proteome analysis of maize roots reveals that oxidative stress is a main contributing factor to plant arsenic toxicity. Phytochemistry. 2005 Jul;66(13):1519-28. Maize seedlings were fed hydroponically with 300 microM arsenate or 250 microM sodium arsenite for 24 h, and changes in differentially displayed proteins were studied by two-dimensional electrophoresis and digital image analysis. The set of identified maize root proteins highly responsive to arsenic exposure included a major and functionally homogeneous group of seven enzymes involved in cellular homeostasis for redox perturbation (e.g., three superoxide dismutases, two peroxidases, one peroxiredoxin, and one reductase) besides four additional, functionally heterogeneous, proteins (e.g., ATP synthase, synthetase, cytochrome P450 and guanine nucleotide-binding protein beta subunit). |
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| 2469630 | Burdon RH, Gill VM, Rice-Evans C: Oxidative stress and heat shock protein induction in human cells. Free Radic Res Commun. 1987;3(1-5):129-39. Agents which induce heat shock protein synthesis in cultured monolayers of Hela cells such as hyperthermia, and sodium arsenite can also cause increases in the levels of lipid peroxidation as determined by the formation of TBA-products. In vitro studies indicate possible damage to ribosomes, and since the heat induced loss of protein synthetic capacity can be increased by superoxide dismutase inhibitors, and prevented by such effects may be linked to the increases observed in lipid peroxidation. |
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| 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. |
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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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| 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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| 2139653 | Kapoor M, Sreenivasan GM, Goel N, Lewis J: Development of thermotolerance in Neurospora crassa by heat shock and other stresses eliciting peroxidase induction. J Bacteriol. 1990 May;172(5):2798-801. Hyperthermia, CdCl2, sodium arsenite, and H2O2 led to the rapid appearance of high levels of peroxidase in Neurospora crassa cultures and induced tolerance toward normally lethal temperatures in 60-h-old colonies. |
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