ccl4中毒大鼠肝脏乙醇代谢的改变:用离体肝灌注系统分析。

Substance and alcohol actions/misuse Pub Date : 1982-01-01
T Yuki, T Hashimoto, K Kuriyama, T Ogasawara, T Takino
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引用次数: 0

摘要

采用非循环无血红蛋白肝灌注系统研究了四氯化碳处理动物肝脏中乙醇代谢的变化。在急性(24小时)后,ccl4使肝脏对乙醇的摄取降低到对照组的56%和30%。治疗后(8-12周)和慢性治疗后(8-12周)。此外,4 mM果糖(一种众所周知的增加肝脏中乙醇代谢的物质)并没有增加ccl4处理的肝脏对乙醇的摄取。肝酒精脱氢酶活性在急性和慢性CCl4治疗后没有改变。乳酸/丙酮酸(胞质NADH/NAD)比值和β -羟基丁酸/乙酰乙酸(线粒体NADH/NAD)比值显著升高,而肝脏摄氧量和线粒体NADH氧化均显著降低,与CCl4诱导肝损伤的程度平行。组织学研究显示急性期肝脏小叶中心凝固性坏死伴脂肪滴形成,慢性期可见中央和门静脉区间的桥接性纤维化及线粒体明显改变的肝硬化模式。这些数据表明,ccl4处理通过抑制NADH再氧化显著降低肝脏乙醇代谢,NADH是肝脏乙醇代谢的限速步骤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Alteration of hepatic ethanol metabolism in CCL4-intoxicated rats: analysis using isolated liver perfusion system.

Hepatic ethanol metabolism in the liver from carbon tetrachloride (CCl4)- treated animals was studied using non-recirculating hemoglobin-free liver perfusion system. CCl4-administration decreased ethanol uptake by the liver to 56% and 30% of the control values following the acute (24 hrs. after treatment) and chronic (8-12 weeks) treatments, respectively. In addition, 4 mM fructose, a well-known agent to increase ethanol metabolism in the liver, did not increase the hepatic uptake of ethanol in CCl4-treated livers. Hepatic alcohol dehydrogenase activity was not changed following acute and chronic CCl4 treatments. The lactate/pyruvate (cytosolic NADH/NAD) ratio as well as beta-hydroxybutyrate/acetoacetate (mitochondrial NADH/NAD) ratio significantly increased, whereas both hepatic oxygen uptake and oxidation of NADH in mitochondria remarkably decreased in parallel with the magnitude of liver injury induced by CCl4. Histological studies revealed that the liver had centrilobular coagulative necrosis with fatty droplet formations at acute phase, while bridging fibrosis between central and portal areas and the pattern of cirrhosis with conspicuous changes in the mitochondria were seen at chronic phase. These data indicate that CCl4-treatment significantly reduces hepatic ethanol metabolism via the inhibition of reoxidation of NADH, a rate limiting step of ethanol metabolism in the liver.

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