Department of Biochemistry, Basic Medical Science Block, Panjab University, Chandigarh 160014, India.
Toxicol Mech Methods. 2010 Mar;20(3):119-26. doi: 10.3109/15376511003606253.
The present study investigates the propensity of atrazine to induce oxidative stress and its possible attenuation by vitamin E in rat erythrocytes, which is a convenient model to understand the oxidative damage induced by various xenobiotics. Experimental animals were administered atrazine (300 mg/kg body weight, daily) and/or vitamin E (100 mg/kg body weight, daily) orally for a period of 7, 14, and 21 days. Results indicated that the reduced glutathione (GSH) content of the erythrocytes of atrazine treated rats was significantly decreased as compared to the control group. Co-administration of vitamin E along with atrazine restored the GSH content of erythrocytes nearly to control levels. The activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione-s-transferase were found to be increased significantly in the erythrocytes accompanied by a decrease in the activity of the glucose-6-phosophate dehydrogenase, following atrazine exposure. On the other hand, when vitamin E was co-administered along with atrazine, activities of these enzymes were found to be restored significantly. In conclusion, results of the study demonstrated that atrazine induced oxidative stress in rat erythrocytes, in terms of increased activities of the various antioxidant enzymes, and decreased content of reduced glutathione. However, vitamin E administration ameliorated the effects of atrazine, suggesting that vitamin E is a potential antioxidant against atrazine-induced oxidative stress.
本研究旨在探讨莠去津诱导大鼠红细胞产生氧化应激的倾向，以及维生素 E 对其的可能缓解作用。大鼠红细胞是研究各种外源化学物诱导氧化损伤的方便模型。实验动物每日经口给予莠去津（300mg/kg 体重）和/或维生素 E（100mg/kg 体重），连续 7、14 和 21 天。结果表明，与对照组相比，莠去津处理组大鼠红细胞的还原型谷胱甘肽（GSH）含量显著降低。同时给予维生素 E 可使红细胞 GSH 含量恢复至接近对照水平。超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶等抗氧化酶的活性在暴露于莠去津后显著升高，同时葡萄糖-6-磷酸脱氢酶的活性降低。另一方面，当同时给予维生素 E 和莠去津时，这些酶的活性被发现显著恢复。总之，该研究结果表明，莠去津通过增加各种抗氧化酶的活性和降低还原型谷胱甘肽的含量，在大鼠红细胞中诱导氧化应激。然而，维生素 E 的给予可改善莠去津的作用，提示维生素 E 是一种对抗莠去津诱导氧化应激的潜在抗氧化剂。
