Pawlosky R J, Salem N
Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcoholism and Alcohol Abuse, Rockville, Maryland 20852, USA.
Alcohol Clin Exp Res. 1999 Feb;23(2):311-7.
Rhesus monkeys that were maintained on an adequate diet but with low levels of essential fatty acids (1.4 en% linoleic, 18:2n-6, and 0.08 en%, linolenic acid, 18:3n-3) became depleted of 20:4n-6, and 22: 6n-3 in their livers, plasma lipoproteins, and erythrocytes during an 18-month period of alcohol exposure (2.6 g kg(-1) day(-1)). Monkeys that consumed alcohol also had higher plasma concentrations of 4-hydroxynonenal compared to controls. The metabolism of 18:2n-6 and 18:3n-3 were evaluated in both groups of animals using deuterium-labeled substrates over a 9-day period. Alcohol consumption did not appear to have an effect on the absorption of either 2H5-18:2n-6 or 2H5-18:3n-3 ethyl esters into the circulation after a single oral dose. However, there was a greater enrichment of deuterium in the biosynthesized fatty acids, 20:4n-6 and 22:6n-3, in the plasma of the monkeys exposed to alcohol compared to controls. These results suggest that chronic alcohol exposure may lead to a stimulation of the rate at which long-chain polyunsaturated fatty acids are biosynthesized to compensate for an increase in lipid peroxidation.
在为期18个月的酒精暴露期（2.6克/千克/天）内，食用充足饮食但必需脂肪酸水平较低（亚油酸1.4%，18:2n-6；亚麻酸0.08%，18:3n-3）的恒河猴，其肝脏、血浆脂蛋白和红细胞中的20:4n-6和22:6n-3减少。与对照组相比，饮酒的猴子血浆中4-羟基壬烯醛的浓度也更高。在9天的时间里，使用氘标记的底物对两组动物的18:2n-6和18:3n-3的代谢进行了评估。单次口服给药后，饮酒似乎对2H5-18:2n-6或2H5-18:3n-3乙酯进入循环的吸收没有影响。然而，与对照组相比，暴露于酒精的猴子血浆中生物合成的脂肪酸20:4n-6和22:6n-3中的氘富集程度更高。这些结果表明，慢性酒精暴露可能会刺激长链多不饱和脂肪酸的生物合成速率，以补偿脂质过氧化的增加。
