Geer B W, McKechnie S W, Langevin M L
Biochem Genet. 1986 Feb;24(1-2):51-69. doi: 10.1007/BF00502978.
At a moderate concentration (2.5%, v/v) dietary ethanol reduced the chain length of total fatty acids (FA) and increased the desaturation of short-chain FA in Drosophila melanogaster larvae with a functional alcohol dehydrogenase (ADH). The changes in length in total FA were postulated to be due to the modulation of the termination specificity of fatty acid synthetase. Because the ethanol-stimulated reduction in the length of unsaturated FA was blocked by linoleic acid, it was thought to reflect the properties of FA 9-desaturase. Although the ethanol-stimulated reduction in chain length of unsaturated FA was also observed in ADH-null larvae, ethanol promoted an increase in the length of total FA of the mutant larvae. Thus, the ethanol-stimulated change in FA length was ADH dependent but the ethanol effect on FA desaturation was not. Ethanol also stimulated a decrease in the relative amount of phosphatidylcholine and an increase in phosphatidylethanolamine. Because similar ethanol-induced changes have been found in membrane lipids of other animals, ethanol may alter the properties of membranes in larvae. It is proposed that ethanol tolerance in D. melanogaster may be dependent on genes that specify lipids that are resistant to the detrimental effects of ethanol.
在适度浓度（2.5%，v/v）下，饮食中的乙醇可缩短黑腹果蝇幼虫中总脂肪酸（FA）的链长，并增加具有功能性乙醇脱氢酶（ADH）的幼虫中短链FA的去饱和度。总FA链长的变化被推测是由于脂肪酸合成酶终止特异性的调节所致。由于乙醇刺激引起的不饱和FA链长缩短被亚油酸阻断，因此认为这反映了FA 9-去饱和酶的特性。尽管在无ADH的幼虫中也观察到乙醇刺激引起的不饱和FA链长缩短，但乙醇促进了突变幼虫总FA链长的增加。因此，乙醇刺激引起的FA链长变化依赖于ADH，但乙醇对FA去饱和度的影响并非如此。乙醇还刺激了磷脂酰胆碱相对含量的降低和磷脂酰乙醇胺的增加。由于在其他动物的膜脂中也发现了类似的乙醇诱导变化，乙醇可能会改变幼虫膜的特性。有人提出，黑腹果蝇的乙醇耐受性可能取决于指定对乙醇有害影响具有抗性的脂质的基因。
