Lefkowith J B, Evers A S, Elliott W J, Needleman P
Prostaglandins Leukot Med. 1986 Aug;23(2-3):123-7. doi: 10.1016/0262-1746(86)90174-5.
Essential fatty acid (EFA) deficiency is a useful tool to study the role of arachidonate and its metabolites in various physiologic and pathologic states. Recent studies have clarified the effects of EFA deficiency on membrane arachidonate and its metabolites, and have demonstrated that 20:3(n-9) (which accumulates in EFA deficiency) can be metabolized to a variety of eicosanoids. EFA deficiency has been shown to exert an anti-inflammatory effect. The mechanism of this effect may in part be mediated through a decrease in leukocyte leukotriene formation. In contrast, studies using the novel fatty acid, columbinic acid, have shown that the epidermal dysfunction seen in EFA deficiency may be a function of linoleate and its lipoxygenase metabolites rather than of arachidonate and the prostaglandins. Finally, it has recently been shown that EFA deficiency potentiates the effects of volatile anesthetics. EFA deficiency may thus provide a useful tool to investigate the molecular mechanism of these drugs.
必需脂肪酸（EFA）缺乏是研究花生四烯酸及其代谢产物在各种生理和病理状态下作用的有用工具。最近的研究阐明了EFA缺乏对膜花生四烯酸及其代谢产物的影响，并表明20:3（n-9）（在EFA缺乏时积累）可代谢为多种类二十烷酸。已证明EFA缺乏具有抗炎作用。这种作用机制可能部分是通过白细胞白三烯生成的减少介导的。相反，使用新型脂肪酸——野芝麻酸的研究表明，EFA缺乏时出现的表皮功能障碍可能是亚油酸及其脂氧合酶代谢产物的作用，而非花生四烯酸和前列腺素的作用。最后，最近已表明EFA缺乏会增强挥发性麻醉剂的作用。因此，EFA缺乏可能为研究这些药物的分子机制提供有用的工具。
