RELEASE AND STEROIDOGENIC ACTIONS OF POLYUNSATURATED FATTY-ACIDS IN THE GOLDFISH TESTIS

The aim of the present study was to examine the role of several polyun saturated fatty acids (PUFA) in the control of steroidogenesis in the goldfish testis. The release of fatty acids from testis tissue in resp onse to the protein kinase C activator phorbol-12-myristate-13-acetate (PMA) and calcium ionophore A23187 was studied. After a 2-h incubatio n, goldfish testis tissue released detectable amounts of several fatty acids, particularly docosahexaenoic acid (DHA). Treatment with PMA (1 00 nM) and A23187 (1 mu M) increased the release of arachidonic acid ( AA) and, to a lesser extent, of eicosapentaenoic acid (EPA). Further e xperiments showed that AA (100 and 400 mu M) and, to a lesser extent, eicosatrienoic acid (ETA; 400 mu M)-but not EPA or DHA (both 400 mu M) -stimulated testicular testosterone (T) production via an indomethacin (INDO; 40 mu M)-sensitive pathway, suggesting that these effects may be mediated through conversion to prostaglandins (FG). E-series PGs fo rmed directly from ETA, AA, or EPA (PGE(1), PGE(2), or PGE(3), respect ively) all stimulate T production, with relative potencies of PGE(2) > PGE(1) > PGE(3). The inability to detect ETA release from testis incu bates and the limited effect of EPA on steroid production suggest that PGE, represents the predominant E-series PG formed under physiologica l conditions in the goldfish testis. The steroidogenic action of AA wa s blocked by treatment with EPA or DHA, acid this effect is due, partl y, to inhibition of PGE(2) formation from AA. EPA or DHA also blocked steroidogenesis stimulated by PGE(2), suggesting a site of action on A A-stimulated T production beyond PGE(2) production. EPA or DHA inhibit ed hCG-stimulated T production by blocking cAMP formation. In summary, the results of the present study demonstrate the opposing effects of n-3 and n-6 series fatty acids on testicular steroid production in the goldfish. The n-6 fatty acid AA stimulates T production, whereas n-3 fatty acids, particularly EPA, may function as inhibitory regulators o f steroid production.