Ryle P R, Chakraborty J, Thomson A D
Dept. of Chemical Pathology, Greenwich District Hospital, London, England.
Alcohol Alcohol Suppl. 1987;1:289-93.
Cysteine and the synthetic antioxidants butylated hydroxytoluene (BHT) and N,N'-diphenyl-phenylenediamine (DPPD) have been found to protect against the increase in hepatic triglycerides caused by acute ethanol administration (2 g/kg/i.p.) in rats. None of these agents affected the ethanol-induced increase in the hepatic redox-state, measured as lactate/pyruvate and 3-hydroxybutyrate/acetoacetate ratios, and there was no influence of any of the compounds on ethanol metabolism. Of the three agents tested, only cysteine was found to lower the liver acetaldehyde concentration after ethanol administration, confirming reports that trapping of acetaldehyde can protect against ethanol hepatotoxicity. The protective action of the anti-oxidants suggests that lipid peroxidation (probably initiated by acetaldehyde) is an important event in the pathogenesis of acute alcoholic fatty liver.
已发现半胱氨酸以及合成抗氧化剂丁基羟基甲苯（BHT）和N，N'-二苯基对苯二胺（DPPD）可防止大鼠急性乙醇给药（2 g/kg/腹腔注射）引起的肝脏甘油三酯增加。这些药物均未影响乙醇诱导的肝脏氧化还原状态的增加，以乳酸/丙酮酸和3-羟基丁酸酯/乙酰乙酸酯比率衡量，并且任何一种化合物对乙醇代谢均无影响。在测试的三种药物中，仅发现半胱氨酸可降低乙醇给药后的肝脏乙醛浓度，证实了乙醛捕获可预防乙醇肝毒性的报道。抗氧化剂的保护作用表明脂质过氧化（可能由乙醛引发）是急性酒精性脂肪肝发病机制中的一个重要事件。
