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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。
Acute oral exposure in rats was used to study the effects of vitamin E (VE) and glutathione (GSH) synthesis inducer (I) -2-oxo-4-hydrothiazole-4-carboxylate (OTC) Blocking Effect of Ethanol (CE) on Lipid Peroxidation. The results showed that VE could restore the content of MDA in liver and plasma to the level of control group; the activity of hepatic glucose-6-Pase and Cyt-P_ (459) and Serum glycocholic acid content and hepatic dyslipidemia and other changes, returned to normal or near normal levels, and mitochondrial succinate dehydrogenase activity failed to return to normal levels. OTC preconditioning can effectively reduce the lipid peroxidation of CE, and the liver G-6-Pase activity and Cyt-P 450 levels decreased, lipid metabolism disorders and other changes were restored to near normal levels. Mitochondrial succinate dehydrogenase (SDH) activity and serum glycocholic acid (SCG) content also significantly improved. OTC was not given until 2 hours after CE exposure.