Androgen synthesis modulation by prostaglandin E2 is differentially mediated via adenylate cyclase and phospholipase C in the testis of the crested newt, Triturus carnifex: in vitro studies.

To study the possible postreceptor mechanisms of prostaglandin E2 in modulating the male newt Triturus carnifex androgen synthesis, during reproduction, testes were in vitro superfused with medium alone, prostaglandin E2, protein kinase C activator (phorbol-12-myristate-13-acetate), prostaglandin E2 plus protein kinase C inhibitor (staurosporine), prostaglandin E2 plus phospholipase C inhibitor (compound 48/80), cAMP analog (dibutyryl cAMP), adenylate cyclase activator (forskolin), prostaglandin E2 plus AC inhibitor (2-0-methyladenosine), prostaglandin E2 plus protein kinase A inhibitor (H-89). In January (reproduction beginning), prostaglandin E2 and phorbol-12-myristate-13-acetate increased androgens, while staurosporine and compound 48/80 counteracted the prostaglandin E2 effect. In March (reproduction ending), prostaglandin E2, dibutyryl cAMP and forskolin decreased androgens, while 2-0-methyladenosine and H-89 counteracted the prostaglandin E2 effect. These data suggest that in Triturus carnifex prostaglandin E2 increases testicular androgens synthesis via phospholipase C at reproduction beginning; on the contrary, this prostaglandin decreases androgens via adenylate cyclase at reproduction ending.