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亚慢性砷和敌敌畏暴露对大鼠红细胞抗氧化防御系统及脂质过氧化的影响

Sub-chronic exposure to arsenic and dichlorvos on erythrocyte antioxidant defense systems and lipid peroxidation in rats.

作者信息

Dwivedi Nidhi, Flora S J S

出版信息

J Environ Biol. 2015 Mar;36(2):383-91.

Abstract

The effect of combined exposure to arsenic (25 ppm in drinking water) and dichlorvos (2.5 mg kg1, orally) for 56 days on biochemical variables, indicative of lipid peroxidation, antioxidant enzyme system and AChE activity in erythrocytes of rats, were examined. While arsenic caused a significant increase in AChE, DDVP produced marked depletion. Combined exposure to arsenic and DDVP produced no additional decrease in AChE activity, which was comparable to DDVP. Arsenic and DDVP also increased the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS), suggesting free radical generation. Interestingly, glutathione linked enzymes (GSH, GPx, GST and GR) significantly increased on arsenic and DDVP exposure. SOD activity also increased significantly in the individually exposed groups, while catalase activity remained unchanged. Blood arsenic level increased significantly on coexposure to arsenic alone and with DDVP exposed group. However, arsenic content in co-exposed group depleted marginally as compared to arsenic alone group, indicating possible arsenic redistribution. It might be concluded from the study that the combined exposure to arsenic and DDVP may lead to synergistic effects on certain biochemical indicators of oxidative stress like ROS, GSH and SOD, suggesting a more pronounced induction of lipid peroxidation in erythrocytes.

摘要

研究了大鼠红细胞中,同时暴露于砷(饮用水中25 ppm)和敌敌畏(2.5 mg/kg,口服)56天对指示脂质过氧化、抗氧化酶系统和乙酰胆碱酯酶(AChE)活性的生化变量的影响。砷使AChE显著增加,而敌敌畏则使其显著降低。同时暴露于砷和敌敌畏并未使AChE活性进一步降低,其降低程度与敌敌畏单独作用时相当。砷和敌敌畏还增加了活性氧(ROS)和硫代巴比妥酸反应性物质(TBARS)的水平,表明产生了自由基。有趣的是,谷胱甘肽相关酶(GSH、GPx、GST和GR)在暴露于砷和敌敌畏时显著增加。单独暴露组的超氧化物歧化酶(SOD)活性也显著增加,而过氧化氢酶活性保持不变。单独暴露于砷组以及同时暴露于砷和敌敌畏组的血砷水平均显著升高。然而,与单独暴露于砷组相比,同时暴露组的砷含量略有下降,表明可能存在砷的重新分布。从该研究可以得出结论,同时暴露于砷和敌敌畏可能对氧化应激的某些生化指标如ROS、GSH和SOD产生协同作用,提示红细胞中脂质过氧化的诱导作用更为明显。

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