Mahadevappa V G, Holub B J
Department of Nutritional Sciences, University of Guelph, Ontario, Canada.
J Lipid Res. 1987 Nov;28(11):1275-80.
The thrombin-dependent losses of eicosapentaenoate (EPA) from the various phospholipids of platelets derived from human subjects ingesting a fish lipid concentrate (MaxEPA) were quantitatively assessed and studied in relation to arachidonate (AA). The net loss of AA and EPA from the total phospholipid, phosphatidylcholine (PC) + phosphatidylethanolamine (PE) + phosphatidylserine (PS) + phosphatidylinositol (PI) (loss from phosphatidylinositol minus accumulated phosphatidate), amounted to 44.4 and 7.3 nmol/2 x 10(9) platelets (mean values, n = 4 subjects), respectively, in response to thrombin (2 units/ml). The phosphatidylcholine, phosphatidylethanolamine (including alkenylacyl), phosphatidylserine, and phosphatidylinositol contributed 46, 17, less than 5, and 33%, respectively, of the AA loss; in contrast to these distributions, the corresponding phospholipid contributions to the net loss of EPA were 71, 27, less than 1, and less than 2%, respectively. Furthermore, the inhibition of AA- and EPA-phospholipid degradation by trifluoperazine indicated that almost all of the release of EPA occurs from PC and PE (greater than 95% of total EPA loss) upon thrombin stimulation and is mediated predominantly via phospholipase A2 activity with almost no contribution from PI. Similarities in the molar ratios of AA/EPA in the PC (3.9) or PE (3.7) which were degraded with those in the corresponding phospholipids from resting platelets suggested no marked selectivity by the phospholipase A2 in intact thrombin-stimulated human platelets in the hydrolysis of AA-PC (or AA-PE) versus EPA-PC (or EPA-PE). Quantitation of the newly released free AA and EPA was determined in the presence of BW755C, a dual cyclooxygenase/lipoxygenase inhibitor which was found not to influence the degradation of individual AA- and EPA-containing phospholipids.(ABSTRACT TRUNCATED AT 250 WORDS)
对摄入鱼类脂质浓缩物（MaxEPA）的人体受试者血小板中各种磷脂的凝血酶依赖性二十碳五烯酸（EPA）损失进行了定量评估，并与花生四烯酸（AA）相关联进行了研究。在凝血酶（2单位/毫升）作用下，总磷脂（磷脂酰胆碱（PC）+磷脂酰乙醇胺（PE）+磷脂酰丝氨酸（PS）+磷脂酰肌醇（PI），磷脂酰肌醇损失减去积累的磷脂酸）中AA和EPA的净损失分别为44.4和7.3纳摩尔/2×10⁹个血小板（平均值，n = 4名受试者）。磷脂酰胆碱、磷脂酰乙醇胺（包括烯基酰基）、磷脂酰丝氨酸和磷脂酰肌醇对AA损失的贡献分别为46%、17%、小于5%和33%；与这些分布相反，相应磷脂对EPA净损失的贡献分别为71%、27%、小于1%和小于2%。此外，三氟拉嗪对AA和EPA磷脂降解的抑制表明，凝血酶刺激后，几乎所有EPA的释放都发生在PC和PE中（占总EPA损失的95%以上），并且主要通过磷脂酶A2活性介导，PI几乎没有贡献。降解的PC（3.9）或PE（3.7）中AA/EPA的摩尔比与静息血小板相应磷脂中的摩尔比相似，这表明完整的凝血酶刺激的人体血小板中的磷脂酶A2在水解AA-PC（或AA-PE）与EPA-PC（或EPA-PE）时没有明显的选择性。在双环氧化酶/脂氧合酶抑制剂BW755C存在下对新释放的游离AA和EPA进行了定量，发现该抑制剂不影响单个含AA和EPA磷脂的降解。（摘要截断于250字）
