DESATURATION OF ESSENTIAL FATTY ACIDS USING STABLE ISOTOPE GC-MS

已经发现，长期的乙醇消费会降低 多不饱和脂肪酸，特别是20：4n6（花生四烯酸），和 22：6n3（二十二碳六烯酸），血浆脂蛋白，红细胞， 灵长类动物和猫科动物的肝脏、大脑和视网膜维持在低水平， 必需脂肪酸饮食（在中枢神经系统中，22：6n3是主要的脂肪酸） 酸减少）。 生成脂肪酸20：4n6和22：6n3， 从必需脂肪酸（EFA），亚油酸（18：2n6）和亚麻酸 (18：3n3）。 稳定同位素气相色谱-质谱 光谱法（GC-MS）方法被用来检查的影响， 乙醇对体内多不饱和脂肪酸产生的影响。 以来 脂质过氧化作用可能在消耗 多不饱和脂肪酸、4-羟基烯醛和 还使用GC-MS监测组织中的8-异前列烷-F（2）-α 程序. 结合代谢研究，神经功能在 使用视网膜电描记术来研究视网膜的水平。 一直在消耗乙醇的灵长类动物（平均占能量的24%） 四年来，每天都有明显的酒精诱导肝脏 病理学，包括脂肪变性、炎症、细胞周和小静脉 纤维化 血浆20：4n6和22：6n3水平降低 脂蛋白、红细胞和肝磷脂。 在大脑里 22：6n3和22：5n6水平降低，22：5n6水平代偿性升高 程度. 体内EFA代谢研究表明， 18：3n3或18：2n6进入血浆在两种对照中大致相同， 酒精暴露的动物 脂质过氧化反应， 血浆中4-羟基壬烯醛和8-异前列烷-F（2）-α的水平 似乎是导致组织减少的主要原因 多不饱和脂肪酸 与视觉功能相关的神经过程 也受到了影响，因为有重大变化， 与对照组相比，暴露于酒精的灵长类动物的视网膜电图。

Prolonged ethanol consumption has been found to lower the levels of polyunsaturated fatty acids especially, 20:4n6 (arachidonic acid) and 22:6n3 (docosahexaenoic acid), in plasma lipoproteins, erythrocytes, livers, brains, and the retinas of primates and felines maintained on low essential fatty acid diets (in the CNS, 22:6n3 is the principal fatty acid which decreased). The fatty acids, 20:4n6 and 22:6n3, are produced from the essential fatty acids (EFA), linoleate (18:2n6) and linolenate (18:3n3), respectively. A stable isotope gas chromatography-mass spectrometry (GC-MS) method is being used to examine the effects of ethanol on the production of polyunsaturated fatty acids in vivo. Since lipid peroxidation may play a particular role in the depletion of polyunsaturated fatty acids, the levels of 4-hydroxyalkenals and the 8-isoprostane-F(2)-alpha, in tissues are also being monitored using GC-MS procedures. In conjunction with metabolism studies, neural function at the level of the retina is being studied using electroretinography. Primates that have been consuming ethanol (on average 24% of energy) daily for four years have developed significant alcohol-induced liver pathology, including steatosis, inflammation, pericellular, and venular fibrosis. The levels of 20:4n6 and 22:6n3 decreased in plasma lipoproteins, erythrocytes, and liver phospholipids. In the brains there were lower levels of 22:6n3 and and a compensatory increase in 22:5n6 levels. In vivo EFA metabolism studies indicated that the uptake of 18:3n3 or 18:2n6 into the plasma was about the same in both controls and alcohol-exposed animals. Lipid peroxidation as evidenced by higher levels of 4-hydroxynonenal and 8-isoprostane-F(2)-alpha in the plasma appear to be a primary cause which leads to decreases in tissue polyunsaturated fatty acids. Neural processes related to visual function were also effected since there were significant alterations in the electroretinograms of alcohol-exposed primates compared to controls.