Abstract

Consumption of n-3 polyunsaturated fatty acids (n-3 PUFAs) is associated with a reduced incidence of coronary arterial diseases. Dietary n-3 PUFAs act via several mechanisms. They depress plasma lipids, especially triglycerides (TGs), by inhibiting hepatic TGs and possibly apoprotein synthesis. They replace arachidonic acid (AA) in phospholipid pools with eicosapentaenoic acid (EPA) and docosahexaenoic acids (DHA). EPA and DHA, when released, inhibit cyclooxygenase and lipoxygenase and reduce eicosanoid synthesis, particularly thromboxane (TXA2) and leukotriene B4 (LTB4), by platelets and macrophages. Reduction of the proaggregatory, vasoconstrictive TXA2 decreases the thrombotic tendency of platelets. This is augmented by the limited depression of the vasoactive antiaggregatory prostacyclin (PGI2) and the generation of antiaggregatory prostaglandin I3 (PGI3) from EPA. The n-3 PUFAs also depress eicosanoid metabolism in platelets, monocytes, and macrophages, and thereby may retard the initiation and progress of atherogenesis. n-3 PUFAs reduce blood pressure and blood viscosity and modulate membrane fluidity and associated enzyme and receptor functions. The collective effects of n-3 PUFAs may account for the reduction in coronary arterial disease in populations consuming foods containing n-3 PUFAs.