氯乙醇急性肝脏毒性研究——Ⅱ 抗氧化剂与谷胱甘肽诱导剂对脂质过氧化形成的影响  

Studies on acute hepatic toxicity of chloroethanol:2. Effect of antioxidant and glutathione inducer on lipid-peroxidation of chloroethanol

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》1993年第3期144-148,共5页Journal of Health Toxicology

摘　　要：利用大鼠急性经口染毒模型研究了维生素E(VE)与谷胱甘肽(GSH)合成诱导剂(一)-2-氧-4-氢噻唑-4-羧酸盐(OTC)对氯乙醇(CE)脂质过氧化效应的阻断作用。结果表明,VE可使肝脏及血浆中MDA含量恢复至对照组水平;肝脏葡萄糖-6-磷酸酶(G-6-Pase)活性、细胞色素P_(450)(Cyt-P_(459))含量及血清甘胆酸含量下降及肝脏脂肪代谢障碍等改变,恢复至正常或接近正常水平,而线粒体琥珀酸脱氢酶活性未能恢复正常水平。 OTC预诱导能有效地减轻CE的脂质过氧化作用,使肝脏G-6-Pase 活性及Cyt-P_(450)含量下降、脂质代谢障碍等改变均恢复至接近正常水平。线粒体琥珀酸脱氢酶(SDH)活性及血清甘胆酸(SCG)含量也有明显改善。在CE染毒2 小时后才给予OTC则效果减弱。Using acute per os intoxicated rat model, the effect of antioxidant and glutathione induc-er (OTC) on intervention of lipid peroxidation of chloroethanol (CE) was studied. The resu-lts showed that Vitamin E treatment restored the melonodialdehyde concentrations levels inliver and plasma to their levels as control. It was also able to reverse the lowered values ofhepatic G-6-Pase activity, cytochrome P450 and SCG levels as well as the disturbed metaboli-sm of hepatic lipid due to CE to normal or nearly normal. However, the activity of mitoch-ondrial SDH though improved obviously, not yet completely recovered. Pre-induction by OTC could not only effectively alleviate the lipid peroxidation due toCE, but also help those indices like hepatic G-6-Pase, Cyto-P450. lipid metabolism resume orapproximate their original level. In addition, the mitochondrial SDH activity and SCG leve-ls were simultaneously greatly improved. OTC treatment given 2 hours after CE dosing re-duced the above effects.

关 键 词：氯乙醇 肝脏毒性 卫生毒理 

分 类 号：R114[医药卫生—卫生毒理学]