百草枯诱导大鼠肝脏氧化应激的研究。

S G Konstantinova, E M Russanov
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引用次数: 0

摘要

以150 mg/kg百草枯(PQ)单次口服大鼠20小时后肝脏氧化损伤为研究对象。PQ对细胞质超氧化物歧化酶(SOD)活性没有影响,但使线粒体SOD活性提高了14%。GSH水平下降30%,GSH/GSSG比值下降近2倍。PQ对线粒体SOD活性的增强与GSH水平的降低之间的相关性暗示了药物肝毒性中O2-的作用。线粒体乌头酶活性略有下降(9%),而细胞质乌头酶活性不受影响。研究结果进一步揭示了两种乌头菌对氧化应激的反应。
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Studies on paraquat-induced oxidative stress in rat liver.

Oxidative injury of liver was studied 20 hr after a single oral administration of 150 mg/kg paraquat (PQ) to rats. PQ exerted no effect on cytosolic superoxide dismutase (SOD) activity but increased mitochondrial SOD activity by 14%. The level of GSH was decreased by 30%, and GSH/GSSG ratio was diminished almost twice. The correlation between the enhancement of mitochondrial SOD activity and the diminution of GSH level by PQ implicates O2- in the liver toxicity of the drug. Mitochondrial aconitase activity was slightly decreased (by 9%) while cytosolic aconitase activity was not affected. The results cast additional light on the responses of both aconitases to oxidative stress.

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