Abstract
Eicosapentaenoic acid (EPA), a major polyunsaturated fatty acid of fish has been widely proposed as a potential nutrient for decreasing platelet-endothelial cell interactions and the subsequent atherogenesis and thrombogenesis. This is mainly based upon the decrease of arachidonic acid (AA) oxygenation into bioactive molecules like thromboxane A 2. In addition, EPA may be oxygenated into its own active derivatives via cell dioxygenases. We report evidence for the requirement of specific peroxides, adequately provided by AA, to allow EPA to be oxygenated into its bioactive products like prostaglandin I 3, a prostacyclin mimetic. On the other hand, we present some data that argue for a decreased basal AA dioxygenation (specific peroxidation) by small concentrations of EPA. The interactions between AA and EPA are then dual, EPA being able to counteract AA oxygenation whereas EPA requires AA to be efficiently oxygenated.
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