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硫丹对雄性大鼠肾脏的毒性与药物代谢酶及微粒体脂质过氧化的关系。

Toxicity of endosulfan on kidney of male rats in relation to drug metabolizing enzymes and microsomal lipid peroxidation.

作者信息

Singh S K, Pandey R S

出版信息

Indian J Exp Biol. 1989 Aug;27(8):725-8.

PMID:2633982
Abstract

Endosulfan administration (po, 15 and 30 days at 7.5 and 10 mg/kg body wt respectively) inhibited the activity of microsomal mixed function oxidases in kidney tissue of male rats. Microsomal and cytosolic protein contents of kidney were significantly increased following 30 days endosulfan exposures. Profound induction in the activity profiles of alcohol dehydrogenase and cytosolic glutathione s-transferase was noticed, however, no such change was apparent in the activity of aldehyde dehydrogenase. Microsomal preparations from treated animals showed a dose and duration dependent increase in spontaneous lipid peroxidation. The observed biochemical changes persisted even after 7 days normalcy allowance provided after the endosulfan (10 mg/kg body wt) withdrawl. The results suggest a substantial renal toxicity of endosulfan to male rats in relation to microsomal mixed function oxidases and associated functions which possibly resulted from lipid peroxidative damage of microsomal membrane in treated animals.

摘要

给予硫丹(经口给药,分别以7.5毫克/千克体重和10毫克/千克体重的剂量给药15天和30天)会抑制雄性大鼠肾组织中微粒体混合功能氧化酶的活性。在硫丹暴露30天后,肾脏的微粒体和胞质蛋白含量显著增加。注意到乙醇脱氢酶和胞质谷胱甘肽S-转移酶的活性谱有显著诱导,但醛脱氢酶的活性没有明显变化。来自处理动物的微粒体制剂显示出自发性脂质过氧化呈剂量和时间依赖性增加。即使在停止给予硫丹(10毫克/千克体重)后给予7天的正常恢复期,所观察到的生化变化仍然存在。结果表明,硫丹对雄性大鼠具有显著的肾脏毒性,这与微粒体混合功能氧化酶及相关功能有关,这可能是由于处理动物的微粒体膜脂质过氧化损伤所致。

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