Arachidonic Acid and Prostaglandin E2 Stimulate Testosterone Production by Goldfish Testis in Vitro

Studies were conducted to determine the effects of arachidonic acid (AA) and its metabolites on testosterone (T) production by goldfish testis pieces. AA (25-400 microM) stimulated a dose-related increase in T production and this effect was potentiated by cyclic nucleotide phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. T production in response to AA was elevated after 2 hr and continued to increase up to 24 hr. The stimulatory effect of AA was strongly inhibited by indomethacin and ibuprofen which block cyclooxygenase activity, whereas nordihydroguaiaretic acid, a lipoxygenase inhibitor, had no effect. Eicosatetraynoic acid, which inhibits both cyclooxygenase and lipoxygenase activity, also attenuated AA-stimulated T production. Together, these results suggest that AA effects on T production are mediated by metabolite(s) of the cyclooxygenase pathway. Several cyclooxygenase products stimulate T production; their relative potency was PGE2 = PGE1 >> PGI2 > PGF2 alpha while PGD2 had no effect. Lipoxygenase products of AA metabolism, including 5-, 11-, 12- and 15-hydroxyeicosatetraenoic acid had no effect on T production. AA, PGE2, and hCG increased cAMP production, suggesting that these compounds mediate T production through the actions of the same signaling molecule. In support of this contention, PGE2 had no additive effect on T production stimulated by a maximal dose of hCG. These data suggest that a cyclooxygenase metabolite of AA, likely PGE2, is involved in the control of steroidogenesis in the goldfish testis.