Salem N, Karanian J W
Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892.
Adv Alcohol Subst Abuse. 1988;7(3-4):183-97. doi: 10.1300/J251v07n03_23.
Ethanol exposure leads to a loss in membrane polyunsaturated fatty acids (PUFA). It is proposed that polyunsaturated species of phospholipids are not randomly distributed, but are concentrated in the cytosolic leaflets of the plasma membrane and are preferentially associated with membrane proteins. These lipids affect the physical state of environments surrounding membrane proteins and thereby serve to regulate many cellular functions. Disruption of these environments may occur even when a small percentage of total polyunsaturates is lost due to ethanol exposure. One possible mechanism of ethanol-induced polyunsaturate loss may be activation of a phospholipase A2 enzyme which is selective for these species of phospholipids. Fatty acids released would stimulate the production of prostaglandins and/or leukotrienes. Similarly, the released docosahexaenoate can be metabolized by rat brain to leukotriene-like compounds which are biologically active in smooth muscle systems. This metabolism is stimulated by ethanol in human platelets, in vitro.
乙醇暴露会导致膜多不饱和脂肪酸（PUFA）的损失。有人提出，磷脂的多不饱和种类并非随机分布，而是集中在质膜的胞质小叶中，并优先与膜蛋白结合。这些脂质会影响膜蛋白周围环境的物理状态，从而调节许多细胞功能。即使由于乙醇暴露导致总多不饱和脂肪酸中有一小部分损失，这些环境也可能受到破坏。乙醇诱导多不饱和脂肪酸损失的一种可能机制可能是激活对这些磷脂种类具有选择性的磷脂酶A2酶。释放出的脂肪酸会刺激前列腺素和/或白三烯的产生。同样，释放出的二十二碳六烯酸可被大鼠大脑代谢为在平滑肌系统中具有生物活性的白三烯样化合物。在体外，乙醇会刺激人血小板中的这种代谢。
