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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。
The acute oral toxicity model of rats was used to study the relationship between the effects of chloroethanol on lipid peroxidation and liver injury. The results showed that the content of malondialdehyde in the medium and high dose groups increased gradually with the prolongation of action time and reached the peak at 12 hours. Liver glucose-6-phosphatase activity and microsomal malondialdehyde content was highly negatively correlated, mitochondrial succinate dehydrogenase activity and mitochondrial malondialdehyde content was highly positively correlated. Serum glycocholic acid content appears first increased and then decreased biphasic response. The content of hepatic reduced glutathione decreased sharply after 1 hour of exposure and returned to its normal level at 12 hours. The main pathological changes in the liver lobular hepatic steatosis of the liver.