黄磷引起肝脏损害机理及部位的研究

Studies on Mechanism and Location of Liver Injury Induced by Yellow Phosphorus

本研究利用黄磷急性、亚急性中毒动物模型发现:黄磷对大鼠急性、亚急性中毒均引起肝匀浆MDA含量显著升高,Schiff碱荧光强度显著增强,肝线粒体和微粒体MDA含量均显著升高,这四项LPO标在急性中毒24h均表现出显著的剂量—效应关系;并伴随肝匀浆TG含量显著升高,肝匀浆GDH含量显著降低,这两项肝脏损害指标的变化与LPO指标的变化存在平行关系或相关关系;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的MDA含量升高存在平行关系或负相关关系。结果表明:黄磷急性、亚急性中毒引起肝脏损害的机理之一是LPO;黄磷急性、亚急性中毒引起肝细胞中的的线粒体和微粒体发生LPO损害作用。

The tats poisoned acutly and subacutly by yellow phoaphorus were studied. In the poisoned rats, the contents of MDA in hepatic homogenate, mitochondria and microsome were found to be significantly increased. The significant rise was found in fluorescent intensity of Schiff base in hepatic homogenate. The four indices of lipid peroxidation show significant dose—effect relationships in the rats poisoned acutly by yellow phosphorus at 24 hours. The significances were found in the increases of hepatic TG contents and in the decreases of hepatic GSH contents. The changes of the two liver injury indices were parallel or correlative relations with the changes of lipid peroxidation indices. 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 relations or negative correlations with the decreases of their enzymes activities respectively. The results suggest that one of mechanisms of liver injury in the rats poisoned acutly and subacutly by yellow phosphous was lipid peroxidation and the injured effects of lipid peroxidation in hepatic mitochondria and mierosome of rats were induced by acute and subacute poisioning of yellow phosphorus.