【摘要】 本文初步探讨了CCl₄致大鼠急性肝损伤的机理。一次经口给予大鼠CCl₄2.5ml/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,CCl₄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。更多还原

【Abstract】 In this study the mechanism of acute liver injury in therats induced by CCl₄ was investigated.The serum ALT and ASTactivities were found to be significantly increased at 12,24,and 48hrs after a single oral dose of CCl₄ at 2.5 ml/kg.Twelve hrs afterthe dose being given,hepatic microsome cytochrome P-450 content inthe rats was markedly reduced.The decrease was found in GSHcontent in hepatic homogenate and glutathione-peroxidase and catalaseactivities in 15,000g pellet prepared from homogenate.The MADcontent in homogenate,mitochondria,and microsome membranes wasfound to be increased,showing time-dependent relationship.Theincrease of MDA content in serum was also observed.The membranefluidity of mitochondria and mierosome was found to be increased andthe fatty acid composition of homogenate changed,in accompanimentwith peroxidation of membrane lipid.These results suggest that the oxidative stress induced by freeradicals which are generated from CCl₄ via catalysis of hepaticcytochrome P-450 may be a mechanism of CCl₄-induced liver injuryin rats.更多还原