Dietary fish and prostanoid formation in man.

Dietary mackerel causes the increase of timnodonic acid (eicosapentaenoic acid) in all platelet phospholipid classes, at the expense of arachidonic acid. Because of these fatty acid changes, the potency of platelets to produce cyclo oxygenase products from the 2-series is greatly reduced. However, upon mild platelet triggering, changes in TxB2 formation are hardly significant, strongly depend on dietary compliance and require a high fish intake. The reduced formation of 2-series prostanoids is only partly compensated for by the increased formation of timnodonic acid-derived products. Urinary PGI metabolites suggest that dietary fish is associated with the enhanced turnover of PGI3 without a concomitant reduction in PGI2 formation. Since the site of PGI formation is not known, and an effect of dietary fish on the prostanoid metabolic routes cannot be excluded, the physiological relevance of these results is uncertain.