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本文初步探讨了CCl_4致大鼠急性肝损伤的机理。一次经口给予大鼠CCl_42.5ml/kg 后12、24和48小时,血清ALT及AST活性显著增高。染毒后12小时,肝微粒体细胞色素P-450含量明显减少。肝匀浆GSH含量以及15000g 沉淀的谷胱甘肽—过氧物酶和过氧化氢酶活性下降。肝匀浆、线粒体和微粒体膜MDA含量增高,且呈时间依赖关系。血清MDA含量也明显增高。与脂质过氧化同时,线粒体和微粒体膜流动性增高;肝匀浆脂肪酸组成发生变化。这些结果提示,CCl_4在肝细胞色素P-450催化下产生自由基,进而导致氧化应激,可能是引起大鼠肝损伤的机理。
In this paper, the mechanism of acute hepatic injury induced by CCl_4 in rats was preliminary investigated. After a single oral administration of CCl_42.5ml/kg to rats at 12, 24 and 48 hours, serum ALT and AST activity increased significantly. 12 hours after exposure, the content of cytochrome P-450 in liver microsomes was significantly reduced. Liver homogenate GSH content and 15,000 g of precipitated glutathione peroxidase and catalase activity decreased. Liver homogenate, mitochondria and microsomal membrane MDA content increased, and a time-dependent relationship. Serum MDA content also increased significantly. Along with lipid peroxidation, the mobility of mitochondria and microsomal membranes increased; fatty acid composition of liver homogenates changed. These results suggest that CCl_4 produces free radicals catalyzed by hepatic cytochrome P-450, which in turn leads to oxidative stress and may be the mechanism that causes liver damage in rats.