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