Department of Biochemistry, Basic Medical Sciences Building, Panjab University, Chandigarh, India.
Environ Toxicol Pharmacol. 2011 May;31(3):378-86. doi: 10.1016/j.etap.2011.01.004. Epub 2011 Feb 4.
Organophosphate (OP) insecticides have been reported to induce oxidative stress due to lipid peroxidation and alteration in defense mechanisms. It is known that calcium content in erythrocytes plays a very important in normal physiology of cells. Erythrocytes are a very convenient model to understand the susceptibility of membrane to oxidative damage induced by various xenobiotic compounds. The aim of present study was to investigate the effects of ethion induced oxidative damage, alterations in membrane bound enzymes and Ca(2+) homeostasis and a possible protective role of vitamin E. Adult male albino rats of Wistar strain were orally administered ethion and vitamin E daily for 28 days. Animals were randomly divided into four groups: control; ethion treated (2.7 mg/kgbw/day); vitamin E treated (50mg/kg of bw/day); ethion+vitamin E treated. The animals were sacrificed after 7, 14, 21 and 28 days. Erythrocyte membranes were prepared and analyzed for protein, lipid peroxidation (LPO) and membrane bound ATPases. Furthermore, Ca(2+) homeostasis as function of time and concentration was evaluated in erythrocytes. The results from the present study show that in vivo administration of ethion resulted in oxidative damage to erythrocyte membranes as evident by increased lipid peroxidation. The increased LPO following ethion intoxication was accompanied by significant decrease in the activities of Na(+)/K(+)-ATPase, Mg(2+)-ATPase and Ca(2+)-ATPase and disturbed Ca(2+)homeostasis in erythrocytes. Furthermore, vitamin E treatment had a beneficial effect by decreasing lipid peroxidation; partially restoring activities of membrane bound ATPases and Ca(2+) homeostasis. The present study suggests that ethion exerts its toxic effect by increasing LPO, altering the activity of membrane bound enzymes and disturbing Ca(2+) homeostasis. Vitamin E treatment ameliorated the toxic effects of ethion suggesting its role as a potential antioxidant.
有机磷（OP）杀虫剂已被报道会由于脂质过氧化和防御机制的改变而引起氧化应激。已知红细胞中的钙含量在细胞的正常生理中起着非常重要的作用。红细胞是了解各种外源化合物诱导的膜氧化损伤易感性的非常方便的模型。本研究旨在研究乙硫磷诱导的氧化损伤、膜结合酶和 Ca（2+）稳态的改变以及维生素 E 的可能保护作用。雄性 Wistar 白化大鼠经口给予乙硫磷和维生素 E，每天一次，共 28 天。动物随机分为四组：对照组；乙硫磷处理组（2.7mg/kgbw/天）；维生素 E 处理组（50mg/kgbw/天）；乙硫磷+维生素 E 处理组。动物在第 7、14、21 和 28 天处死。制备红细胞膜并分析蛋白质、脂质过氧化（LPO）和膜结合 ATP 酶。此外，还评估了红细胞中 Ca（2+）稳态的时间和浓度依赖性。本研究结果表明，乙硫磷体内给药导致红细胞膜氧化损伤，表现为脂质过氧化增加。乙硫磷中毒后 LPO 的增加伴随着 Na（+）/K（+）-ATP 酶、Mg（2+）-ATP 酶和 Ca（2+）-ATP 酶活性的显著降低以及红细胞中 Ca（2+）稳态的紊乱。此外，维生素 E 治疗通过降低脂质过氧化、部分恢复膜结合 ATP 酶的活性和 Ca（2+）稳态来发挥有益作用。本研究表明，乙硫磷通过增加 LPO、改变膜结合酶的活性和扰乱 Ca（2+）稳态发挥其毒性作用。维生素 E 治疗改善了乙硫磷的毒性作用，表明其作为潜在抗氧化剂的作用。
