慢性氟中毒大鼠肝脏损害机理及亚细胞部位研究

用３０ｍｇ／Ｌ，６０ｍｇ／Ｌ和１２０ｍｇ／Ｌ含氟水饲养大鼠１２周，复制慢性氟中毒动物模型，探讨肝脏损害机理和亚细胞部位、结果发现：肝损害指标肝甘油三酯（ＴＧ）含量和血清谷丙转氨酶（ＳＧＰ）活性显著升高；肝雨二醛（ＭＤＡ）含量显著升高，肝还原型谷胱甘肽（ＧＳＨ）含量显著降低；肝脂质过氧化指标变化与肝损害指标变化呈平行关系；肝线粒体和微粒体ＭＤＡ含量显著升高，其相应标志酶琥珀酸脱氢酶（ＳＤＨａｓｅ）和葡萄糖－６－磷酸酶（Ｇ－６－Ｐａｓｅ）活性显著降低，而且各亚细胞器ＭＤＡ含量升高分别与各自标志酶活性降低存在显著负相关关系。结果提示，慢性氟中毒引起肝脏损害机理之一是脂质过氧化；慢性氟中毒可致肝细胞线粒体和微粒体发生脂质过氧化损害作用。

Studies on mechanism and subcellular location of liver injuries caused by chronic fluorosis in rats

The animal model of chronic fluorosis was reproduced by drinking water supplemented with30mg/L, 60mg/L and 120mg/L fluorine for 12 weeks. The mechanism and subcellular location ofliver injuries were studied. The following results were found:The content of hepatic TG and activity of serum SGPT were markedly increased. The significances was found in the increase of hepatic'MDA content and in the decrease of hepatic GSH content. The changes of hepatic lipid petoxidation indeces were patallel with the changes of liver injury indices. The content of MDA in hepatic mitochondria and microsomes were markedly increased. The activities of SDHase in hepatic mitochondria and G-6-Pase in hepatic microsomes were significantly reduced. The increase of MDAcontent in two subcellular parts showed significantly negative correlations to the decreases oftheir enzymes activities, respectively. The results suggest that one of mechanism of liver injuriesin the rats of chronic fluorosis was lipid peroxidation and the injury effects of lipid peroxidation inhepatic mitochondria and microsomes of rats were induced by chronic fluorosis.