Weiner T W, Sprecher H
J Biol Chem. 1985 May 25;260(10):6032-8.
The types of unsaturated fatty acids found in platelet phospholipids must be regulated by a series of controls which include specificity for activation and acylation as well as modification of circulating fatty acids by platelets prior to incubation into phospholipids. In this study we show that washed human platelets not only incorporate [1-14C]6,9,12-18:3, [1-14C]6,9,12,15-18:4, [1-14C]5,8,11-20:3, [1-14C]5,8,11,14-20:4, and [1-14C]5,8,11,14,17-20:5 into their phospholipids but also chain elongate each of these acids with subsequent acylation of the chain elongated products into phospholipids. Platelets incubated alone with 1-14C-labeled 5,8,11-20:3, 5,8,11,14-20:4, 5,8,11,14,17-20:5, 7,10,13,16,19-22:5, or 4,7,10,13,16,19-22:6 incorporated each of these acids into individual phosphoglycerides with phosphatidylinositol having the highest specific activity followed by phosphatidylcholine with phosphatidylserine approximately equal to phosphatidylethanolamine. The incorporation specificity of 4,7,10,13,16,19-22:6 was atypical since it was a relatively poor substrate for acylation into all phospholipids except phosphatidylethanolamine. The 20-carbon acids were better substrates for incorporation into phospholipids than were the 22-carbon compounds. Simultaneous incubation of 10 microM [1-14C]5,8,11,14-20:4 with increasing levels (5 to 15 microM) of each of the above five other 1-14C-labeled acids showed a concentration-dependent increase in the amount of the second fatty acid incorporated into platelet phospholipids. Dietary fat modification thus has the potential of increasing the plasma pool of 22-carbon acids for incorporation into platelets. In addition the activation of 20-carbon eicosanoid precursors by the high affinity platelet activating enzyme (Wilson, D. B., Prescott, S. M. and Majerus, P. W. (1982) J. Biol. Chem. 257, 3510-3515) will yield an acyl-CoA for both acylation and chain elongation followed by subsequent incorporation of 22-carbon acids into phosphoglycerides.
血小板磷脂中不饱和脂肪酸的类型必须通过一系列调控来调节，这些调控包括激活和酰化的特异性，以及血小板在将循环脂肪酸掺入磷脂之前对其进行修饰。在本研究中，我们发现洗涤过的人血小板不仅能将[1-¹⁴C]6,9,12-十八碳三烯酸、[1-¹⁴C]6,9,12,15-十八碳四烯酸、[1-¹⁴C]5,8,11-二十碳三烯酸、[1-¹⁴C]5,8,11,14-二十碳四烯酸和[1-¹⁴C]5,8,11,14,17-二十碳五烯酸掺入其磷脂中，还能使这些酸链延长，并将链延长产物随后酰化到磷脂中。单独用¹⁴C标记的5,8,11-二十碳三烯酸、5,8,11,14-二十碳四烯酸、5,8,11,14,17-二十碳五烯酸、7,10,13,16,19-二十二碳五烯酸或4,7,10,13,16,19-二十二碳六烯酸孵育血小板，这些酸分别都被掺入到各个磷酸甘油酯中，其中磷脂酰肌醇的比活性最高，其次是磷脂酰胆碱，磷脂酰丝氨酸与磷脂酰乙醇胺大致相等。4,7,10,13,16,19-二十二碳六烯酸的掺入特异性是非典型的，因为除了磷脂酰乙醇胺外，它作为酰化进入所有磷脂的底物效果相对较差。二十碳的酸作为掺入磷脂的底物比二十二碳的化合物更好。在10微摩尔1-¹⁴C标记的5,8,11,14-二十碳四烯酸与上述其他五种¹⁴C标记的每种酸的水平增加浓度（5至15微摩尔）的同时孵育，结果显示掺入血小板磷脂中的第二种脂肪酸的量呈浓度依赖性增加。因此，饮食脂肪修饰有可能增加血浆中二十二碳酸以供掺入血小板。此外，高亲和力血小板激活酶（威尔逊，D.B.，普雷斯科特，S.M.和马杰鲁斯，P.W.（1982年）《生物化学杂志》257, 3510 - 3515）对二十碳类花生酸前体的激活将产生用于酰化和链延长的酰基辅酶A，随后二十二碳酸被掺入磷酸甘油酯中。
