多不饱和脂肪酸和乙醇。

N Salem, J W Karanian
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引用次数: 18

摘要

乙醇暴露导致膜多不饱和脂肪酸(PUFA)的损失。多不饱和磷脂不是随机分布的,而是集中在质膜的细胞质小叶中,并优先与膜蛋白相关。这些脂质影响膜蛋白周围环境的物理状态,从而调节许多细胞功能。即使由于乙醇暴露而损失了总多不饱和物的一小部分,也可能发生这些环境的破坏。乙醇诱导多不饱和脂肪酸损失的一个可能机制可能是磷脂酶A2的激活,该酶对这些磷脂具有选择性。脂肪酸的释放会刺激前列腺素和/或白三烯的产生。同样地,释放的二十二碳六烯酸可被大鼠大脑代谢为白三烯样化合物,在平滑肌系统中具有生物活性。体外实验中,人血小板中的乙醇可促进这种代谢。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Polyunsaturated fatty acids and ethanol.

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.

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