氯乙醇急性肝脏毒性研究——Ⅰ.氯乙醇中毒与脂质过氧化效应  

Studies on Acute Hepatic Toxicity of Chloroethanol Ⅰ. Chloroethanol Toxication and Lipid Peroxidation

作　　者：钟沚 周炯亮[1] 庄志雄[1] 陈铁江[1] 周建平[1] 钟小明[1] 

机构地区：[1]中山医科大学卫生学院,广州510089

出　　处：《卫生毒理学杂志》1992年第4期246-248,263,共4页Journal of Health Toxicology

基　　金：国家自然科学基金

摘　　要：用大鼠急性经口染毒模型研究了氯乙醇脂质过氧化效应与其肝损害作用之间的关系。结果表明,中、高剂量组肝匀浆丙二醛含量随作用时间延长而逐步上升,至12小时达到高峰。肝脏萄葡糖-6-磷酸酶活性与微粒体丙二醛含量升高呈高度负相关,线粒体琥珀酸脱氢酶活力则与线粒体丙二醛含量呈高度正相关。血清甘胆酸含量出现先升高后降低的双相反应。肝脏还原型谷胱甘肽含量在染毒1小时后大幅度下降,12小时已恢复正常水平。肝脏主要的病理改变为小叶中央区肝细胞脂肪变性。Using acute P. Os intoxicated rat model, the relationship between lipid peroxidation due to chloroethanol and liver damage was studied. The results revealed that in mediem ( 30mg/ kg ) and high ( 50mg/kg ) dose group, the MDA content in liver homogenate appeared to be gradually increased with time course, and reached the peak value till 12 h. A high negative correlation( r= -0.88 ) was shown between hepatic G-6-Pase activity and microsomal MDA content. On the contrary, a high positive correlation ( r=0.9538) was shown between SDH and MDA in mitochondria. The SCG content seemed to have diphasic reaction characterized by increasing initially and decreasing lately. One hour after intoxication,the hepatic GSH content appeared to be lowered a great deal, and returned to normal till 12 hours. The main pathological changes showed fatty degeneration of liver cells in central zone. It may be concluded that chloroethenol might be able to elicit severe lipid peroxidation in the liver.

关 键 词：氯乙醇 肝 毒性 过氧化脂质 

分 类 号：R114[医药卫生—卫生毒理学]