黄磷中毒性肝损害的机理探讨

本研究表明,肝微粒体混合功能氧化酶参与了黄磷在体内的活化代谢,促进了肝毒作用。肝谷胱甘肽及其酶系参与了黄磷的解毒代谢,当其耗损或失代偿时,可为脂质过氧化或钙泵障碍提供发生条件,所得数据较充分证明:脂质过氧化是黄磷中毒性肝损害十分重要的机理,但不能认为是唯一的机理,它与钙泵障碍的相互关系,值得进一步研究。电镜及组化的研究发现,线粒体和粗面内质网是黄磷的靶细胞器,其功能和结构改变,是各种病理改变的基础。

The mechanisms by which phosphorus induced liver damage.

The mechanisms of hepatotoxicity of phosphorus was studied on different groups of rats intoxicated by phosphorus by either single or multiple doses respectively, Results showed that phosphorus was metabolized by the liver microsomal mixed-function oxidases. Induction of MFO promoted its liver toxic effect. In addition, the liver GSM and related emenzymes participated in detoxification of phosphorus. Exhaustion of GSH and the enzymes was found to be related to be lipid peroxidation or disturbance of hepatocellar Ca~(2+) homeostasis of liver cells. The results indicated that lipid peroxidation was one of the important mechanisms of chemical liver damage by phosphorus. Electronic microscopy and histochemistry demonstrated that the mitochondria and rough endoplasmic reticulum were the target subcellular orgenelles of phosphorus.