Blank M L, Smith Z L, Cress E A, Snyder F
Medical Sciences Division, Oak Ridge Institute for Science and Education (operated by Oak Ridge Associated Universities, TN 37831-0117.
Biochim Biophys Acta. 1994 Oct 6;1214(3):295-302. doi: 10.1016/0005-2760(94)90076-0.
Effects of dietary fish oil ethyl esters and alkyldiacetylglycerols (an ether-linked lipid) on the distribution of subclasses of choline- and ethanolamine-glycerophospholipids as well as effects on highly unsaturated molecular species of ethanolamine plasmalogens from brain, spleen, kidney, lung, and testis of rats were examined. Supplementation of ethyl ester concentrates of n-3 fatty acids had no effect on the distribution of subclasses in any of the tissues. However, the supplements of 1-O-octadec-9'-enyl-2,3-diacetyl-sn-glycerol (diacetates of selachyl alcohol) caused significant increases in the alkylacylglycerophosphocholine and alkylacylglycerophosphoethanolamine subclasses from spleen and lung and in the alkylacylglycerophosphoethanolamine subclass from kidney. Dietary supplements of fish oil ethyl esters reduced the arachidonate-containing species of ethanolamine plasmalogens whereas molecular species having 20:5(n-3), 22:6(n-3), and/or 22:5(n-3) acyl groups were increased in the spleen, lung, and kidneys, but not brain. In testicular tissue from rats fed the fish oil diets, the molecular species of ethanolamine plasmalogens containing 22:5(n-6) acyl groups were reduced. An increase of ethanolamine plasmalogens with 18:1 alk-1-enyl moieties paired with highly unsaturated sn-2 acyl groups were found in the tissues of rats fed the fish oil plus selachyl alcohol diacetate supplements. Rats on the diet containing fish oil ethyl esters had significantly lower [3H]alkyllysoglycerophosphocholine CoA-independent transacylase activity in spleen microsomes than controls. This suggests that supplements of n-3 fatty acids interferes with the transacylation of arachidonate, an event that could seriously impair the release of arachidonate and lysophospholipids (e.g., lyso-PAF) that are precursors of potent bioactive lipid derivatives.
研究了膳食鱼油乙酯和烷基二乙酰甘油(一种醚键连接的脂质)对大鼠脑、脾、肾、肺和睾丸中胆碱甘油磷脂和乙醇胺甘油磷脂亚类分布的影响,以及对乙醇胺缩醛磷脂高度不饱和分子种类的影响。补充n-3脂肪酸乙酯浓缩物对任何组织中的亚类分布均无影响。然而,补充1-O-十八碳-9'-烯基-2,3-二乙酰基-sn-甘油(鲨肝醇二乙酸酯)会导致脾脏和肺中的烷基酰基甘油磷酸胆碱和烷基酰基甘油磷酸乙醇胺亚类以及肾脏中的烷基酰基甘油磷酸乙醇胺亚类显著增加。膳食补充鱼油乙酯会减少乙醇胺缩醛磷脂中含花生四烯酸的种类,而脾脏、肺和肾脏中具有20:5(n-3)、22:6(n-3)和/或22:5(n-3)酰基的分子种类增加,但脑中未增加。在喂食鱼油饮食的大鼠睾丸组织中,含22:5(n-6)酰基的乙醇胺缩醛磷脂分子种类减少。在喂食鱼油加鲨肝醇二乙酸酯补充剂的大鼠组织中,发现具有18:1烯基-1-烯基部分与高度不饱和sn-2酰基配对的乙醇胺缩醛磷脂增加。喂食鱼油乙酯饮食的大鼠脾脏微粒体中[3H]烷基溶血甘油磷酸胆碱辅酶A非依赖性转酰基酶活性显著低于对照组。这表明补充n-3脂肪酸会干扰花生四烯酸的转酰基作用,这一事件可能会严重损害作为强效生物活性脂质衍生物前体的花生四烯酸和溶血磷脂(如溶血血小板活化因子)的释放。