Losses of arachidonic acid in rat liver after alcohol inhalation
Losses of arachidonic acid in rat liver after alcohol inhalation
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DOI：
10.1007/bf02637068
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发表时间：
1996-03-01
期刊：
影响因子：
1.9
通讯作者：
Karanian, J
中科院分区：
文献类型：
--
作者：
Salem, N;Reyzer, M;Karanian, J
本文介绍了一种酒精中毒的动物模型，在该模型中，大鼠通过吸入暴露于酒精，并喂以模拟某些酗酒者的不良饮食的饮食。据推测，酒精的某些病理生理效应与其对必需脂肪酸代谢和重要器官组成的影响有关。使用不含20碳和22碳必需脂肪酸且具有低水平的18碳必需脂肪酸的饮食作为饮食挑战。增加第二次代谢挑战，即，酒精导致组织多不饱和脂肪酸的损失，特别是肝脏花生四烯酸盐。还提出了一种循环吸入酒精12 h/d的方法，该方法也显示出降低肝脏花生四烯酸含量。
This paper presents an animal model of alcoholism in which rats were exposed to alcohol by inhalation and were fed a diet that simulated the poor diet of some alcoholics. It is hypothesized that some of the pathophysiological effects of alcohol are related to its effects on essential fatty acid metabolism and composition of vital organs. A diet that contains no 20- and 22-carbon essential fatty acids and has low levels of 18-carbon essential fatty acids was used as a dietary challenge. Addition of a second metabolic challenge, i.e., alcohol, led to loss of tissue polyunsaturates, particularly liver arachidonate. A method of cycling alcohol inhalation for 12 h/d was also presented, which was also shown to lower liver arachidonic acid content.