The Effect of Dietary Fish Oil Supplementation and in Vitro Collagen Stimulation on Human Platelet Phospholipid Fatty Acid Composition

Abstract

A large body of evidence has recently accumulated linking the ingestion of n−3 fatty acids of marine origin to decreased cardiovascular disease risk (reviews by Herold & Kinsella, 1986, Leaf & Weber, 1988, and Weaver & Holub, 1988). Consumption of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) reduces blood platelet-vessel wall interactions, thereby decreasing the thrombotic potential by reducing the level of esterified arachidonic acid (AA) in platelet phospholipid and replacing it with n−3 polyunsaturated fatty acids, including EPA, DHA, and docosapentaenoic acid (DPA). In addition, EPA and DHA may also competitively inhibit AA metabolism at the cyclooxygenase level and thus decrease the amount of AA metabolites (Needleman et al., 1979). Upon platelet activation, AA is released from the platelet phospholipid by a combination of phospholipase A2 and phospholipase C-mediated activities (Rittenhouse-Simmons & Deykin, 1981). While phospholipase A2 liberates AA directly, phospholipase C produces diacylglycerol from inositol glycerophospholipids which can either be further metabolized to release AA or phosphorylated to form phosphatidic acid (PA). The released AA,is metabolized by cyclooxygenase to 2-series eicosanoids, including thromboxane A2 (Hamberg et al., 1975), a potentiator of platelet aggregation and a vasoconstrictor. The predominant n-3 fatty acid in the platelet phospholipid of seafood consumers, EPA, is also released from phospholipid and can be metabolized by cyclooxygenase to 3-series eicosanoids including the inactive thromboxane A3 (Needleman et al., 1979; Hamberg, 1980; Fischer & Weber, 1983). While DHA does inhibit platelet aggregation (Rao et al., 1983), it has been shown not to be released in significant quantities from platelet phospholipid upon thrombin stimulation (Fischer et al., 1984).