Kale M, Rathore N, John S, Bhatnagar D
School of Biochemistry, D.A. University, Indore, India.
Toxicol Lett. 1999 Apr 12;105(3):197-205. doi: 10.1016/s0378-4274(98)00399-3.
Pyrethroid pesticides are used preferably over organochlorines and organophosphates due to their high effectiveness, low toxicity to non-target organisms and easy biodegradibility. However, it is possible that during the pyrethroid metabolism, there is generation of reactive oxygen species (ROS) and pyrethroids may produce oxidative stress in intoxicated rats. The present study was therefore, undertaken to determine pyrethroid-induced lipid peroxidation (LPO) and to show whether pyrethroid intoxication alters the antioxidant system in erythrocytes. A single dose of cypermethrin and/or fenvalerate (0.001% LD50) was administered orally to rats and the animals were sacrificed at 0, 1, 3, 7 and 14 days of treatment. The results showed that lipid peroxidation (LPO) in erythrocytes increased within 3 days of pyrethroid treatment. The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT). The increase in reduced glutathione (GSH) content in erythrocytes may probably be an initial adaptive response to increased oxidative stress in pyrethroid intoxicated rats. Erythrocytes and serum acetylcholinesterase (AChE) activity was measured in pyrethroid-induced oxidative stress as it may mimic inhibition in target tissues such as muscle and brain. The inhibition in erythrocytes and serum AChE activity was partially relieved over a period of time indicating recovery from pyrethroid intoxication. The increase in erythrocyte LPO correlated with the inhibition in erythrocyte AChE activity and so erythrocyte AChE can be a marker enzyme in pyrethroid toxicity. The results show oxidative stress and alteration in antioxidant enzymes in erythrocytes of pyrethroid intoxicated rats.
由于拟除虫菊酯类杀虫剂高效、对非靶标生物毒性低且易于生物降解，因此比有机氯和有机磷杀虫剂更受青睐。然而，在拟除虫菊酯代谢过程中，有可能产生活性氧（ROS），并且拟除虫菊酯可能在中毒大鼠体内产生氧化应激。因此，本研究旨在确定拟除虫菊酯诱导的脂质过氧化（LPO），并表明拟除虫菊酯中毒是否会改变红细胞中的抗氧化系统。给大鼠口服单剂量的氯氰菊酯和/或氰戊菊酯（0.001% LD50），并在治疗的第0、1、3、7和14天处死动物。结果表明，拟除虫菊酯处理后3天内红细胞中的脂质过氧化（LPO）增加。氧化应激增加导致超氧化物歧化酶（SOD）和过氧化氢酶（CAT）等抗氧化酶的活性增加。红细胞中还原型谷胱甘肽（GSH）含量的增加可能是对拟除虫菊酯中毒大鼠氧化应激增加的一种初始适应性反应。在拟除虫菊酯诱导的氧化应激中测量红细胞和血清乙酰胆碱酯酶（AChE）活性，因为它可能模拟在肌肉和大脑等靶组织中的抑制作用。红细胞和血清AChE活性的抑制在一段时间内部分得到缓解，表明从拟除虫菊酯中毒中恢复。红细胞LPO的增加与红细胞AChE活性的抑制相关，因此红细胞AChE可以作为拟除虫菊酯毒性的标记酶。结果显示了拟除虫菊酯中毒大鼠红细胞中的氧化应激和抗氧化酶的改变。
