Interactions between prostaglandin precursors during their oxygenation by human platelets.

The oxygenation through the prostaglandin synthase complex and the lipoxygenase pathways of the three prostaglandin precursors was investigated in human platelets. These precursors (dihomogammalinolenic (8,11,14-eicosatrienoic; 20:3 (8,11,14)), arachidonic (5,8,11,14-eicosatetraenoic; 20:4 (5,8,11,14)) and 5,8,11,14,17-eicosapentaenoic (20:5 (5,8,11,14,17)) acids) were used alone or simultaneously. We have found that 20:4 (5,8,11,14) increases the oxygenation of 20:3 (8,11,14) by the prostaglandin synthase complex while 20:5 (5,8,11,14,17) decreases the oxygenation of 20:4 (5,8,11,14) by the same enzyme complex. On the other hand, the utilization of 20:5 (5,8,11,14,17) by the prostaglandin synthase complex and the lipoxygenase was markedly enhanced in the presence of 20:3 (8,11,14), 20:4 (5,8,11,14) or both. Besides, the increased concentrations of 20:5 (5,8,11,14,17) failed to enhance its oxygenation to such an extent while the addition of 20:3 (8,11,14) or 20:4 (5,8,11,14) allows the marked potentiation of the 20:5 (5,8,11,14,17) oxygenation at any concentration. This indicates that, to be efficient, the utilization of 20:5 (5,8,11,14,17) by platelet oxygenases needs the presence of 20:3 (8,11,14), 20:4 (5,8,11,14) or their derivatives. In addition, using small concentrations of each prostaglandin precursor close to concentrations presumably released from platelet phospholipids during aggregation, all show the same tendencies. We conclude that the interactions we have observed between prostaglandin precursors during their oxygenation by human platelets could be of primary importance to explain the modifications of platelet reactivity reported after dietary manipulations.