von Schacky C, Siess W, Fischer S, Weber P C
J Lipid Res. 1985 Apr;26(4):457-64.
During long-term dietary n-3 fatty acid supplementation, eicosapentaenoic acid (EPA) is not incorporated into phosphatidylinositol or -serine of human platelets in vivo and is not detectable in phosphatidic acid upon stimulation with thrombin. However, EPA is released from platelet phospholipids and metabolized to thromboxane B3 (TXB3). In contrast, in vitro, platelets incorporate [14C]EPA into phosphatidylinositol, whether they contain endogenous EPA in their cellular lipids or not. Following platelet stimulation, [14C]EPA appears in phosphatidic acid, as free fatty acid, and is transformed to TXB3. We conclude that the fatty acid compositions of platelet phospholipid subclasses are regulated with a high degree of specificity in vivo. Qualitative differences exist between in vivo and in vitro uptake of EPA into platelet phospholipid subclasses. After in vivo incorporation, EPA is released by action of a phospholipase A2.
在长期膳食补充n-3脂肪酸期间，二十碳五烯酸（EPA）在体内不会掺入人血小板的磷脂酰肌醇或磷脂丝氨酸中，并且在用凝血酶刺激后在磷脂酸中无法检测到。然而，EPA会从血小板磷脂中释放出来并代谢为血栓素B3（TXB3）。相比之下，在体外，无论血小板细胞脂质中是否含有内源性EPA，血小板都会将[14C]EPA掺入磷脂酰肌醇中。血小板受到刺激后，[14C]EPA会以游离脂肪酸的形式出现在磷脂酸中，并转化为TXB3。我们得出结论，血小板磷脂亚类的脂肪酸组成在体内受到高度特异性的调节。体内和体外EPA摄取到血小板磷脂亚类之间存在质的差异。在体内掺入后，EPA通过磷脂酶A2的作用释放出来。
