四氯化碳亚急性中毒引起肝脏损害机理及部位

Studies on mechanism and location of liver injury induced by subacute carbon tetrachloride poisoning

利用CCl_4亚急性中毒动物模型发现:CCl_4对大鼠亚急性中毒引起肝匀浆MDA含量显著升高,Schiff碱荧光强度显著增强,并伴随肝匀浆GSH含量显著降低,肝匀浆TG含量显著升高,血清SGPT活性显著增高,这三项肝损害指标变化与LPO指标变化存在平行关系。肝线粒体和微粒体MDA含量均显著升高,肝线粒体标志酶SDHase活性和肝微粒体标志酶G-6-Pase活性均显著降低,且分别与各自亚细胞器MDA含量升高存在平行关系。结果表明:CCl_4亚急性中毒引起肝脏损害的机理之一是LPO;CCl_4亚急性中毒引起肝细胞中的线粒体和微粒体发生LPO损害作用。

The rats poisoned subacutly by CCl_4 were studied. In the poisoned rats, the contents of MDA in hepatic homogenate were found to be significantly increased. The significant rise was found in fluorescent intensity of Schiff base in hepatic homogenate. The significances were found in the decreases of hepatic GSH contents, in the increases of hepatic TG contents and in the increases of serum SGPT. The changes of the three liver injury indices were parallel relation with the changes of lipid peroxidation indices. The contents of MDA in hepatic mitochondria and microsme were found to be significantly increased. The activities of SDHase in hepatic mitochondria and G-6-Pase in hepatic microsome were found to be markedly reduced. The increases of MDA contents in two subcellular fractions were parallel relation with the decreases of their enzymes activities respectively. The results suggest that one of mechanisms of liver injury in the rats poisoned subacutly by CCl_4 was lipid peroxidation and the injury effects of lipid peroxidation in the hepatic mitochondria and microsome of rats were induced by subacute poisoning of CCl_4.