Release and steroidogenic actions of polyunsaturated fatty acids in the goldfish testis

Abstract

The aim of the present study was to examine the role of several polyunsaturated fatty acids (PUFA) in the control of steroidogenesis in the goldfish testis. The release of fatty acids from testis tissue in response to the protein kinase C activator phorbol-12-myristate-13-acetate (PMA) and calcium ionophore A23187 was studied. After a 2-h incubation, goldfish testis tissue released detectable amounts of several fatty acids, particularly docosahexaenoic acid (DHA). Treatment with PMA (100 nM) and A23187 (1 μM) increased the release of arachidonic acid (AA) and, to a lesser extent, of eicosapentaenoic acid (EPA). Further experiments showed that AA (100 and 400 μM) and, to a lesser extent, eicosatrienoic acid (ETA; 400 μM)-but not EPA or DHA (both 400 μM)-stimulated testicular testosterone (T) production via an indomethacin (INDO; 40 μM)-sensitive pathway, suggesting that these effects may be mediated through conversion to prostaglandins (PG). E-series PGs formed directly from ETA, AA, or EPA (PGE1, PGE2, or PGE3, respectively) all stimulate T production, with relative potencies of PGE2 > PGE1 > PGE3. The inability to detect ETA release from testis incubates and the limited effect of EPA on steroid production suggest that PGE2 represents the predominant E-series PG formed under physiological conditions in the goldfish testis. The steroidogenic action of AA was blocked by treatment with EPA or DHA, and this effect is due, partly, to inhibition of PGE2 formation from AA. EPA or DHA also blocked steroidogenesis stimulated by PGE2, suggesting a site of action on AA-stimulated T production beyond PGE2 production. EPA or DHA inhibited 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 of steroid production.