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Effects of a trans isomer of arachidonic acid on rat platelet aggregation and eicosanoid production.

O. Berdeaux,J. Chardigny,J. Sebedio,T. Mairot,D. Poullain,J. Vatele,J. Nöel

Published 1996 in Journal of Lipid Research

ABSTRACT

The addition of a trans isomer of arachidonic acid (20:4 delta 14trans) to rat platelet suspensions inhibited the aggregation induced by 7.5 microM of arachidonic acid. This inhibitory effect of 20:4 delta 14trans was significant at concentrations of 7.5-22.5 microM and the range of inhibition was 20% at an inhibitor/substrate ratio (I/S) 1 to 66% when I/S reached 3. However, the addition of its structural homolog (20:3n-9) or the natural isomer (20:4n-6) did not induce any modification of the platelet aggregation. In parallel, adding 20:4 delta 14trans to the platelet significantly decreased thromboxane B2 and 12-hydroxyheptadecatrienoic acid production. In contrast, the 12-lipoxygenase pathway was stimulated, as 12-hydroxyeicosatetraenoic acid production increased up to 55% when the I/S reached 3. 20:3n-9, not being a substrate of the cyclooxygenase, did not induce any significant modification in the formation of thromboxane B2 and 12-hydroxyheptadecatrienoic acid. 20:4 delta 14t alone did not induce any platelet aggregation. However, this fatty acid was metabolized to a limited extent into two products that have still to be identified. One of them would be a product of the 12-lipoxygenase pathway.

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