ANDROGEN SYNTHESIS MODULATION BY PROSTAGLANDIN-E2 IS DIFFERENTIALLY MEDIATED VIA ADENYLATE-CYCLASE AND PHOSPHOLIPASE-C IN THE TESTIS OF THECRESTED NEWT, TRITURUS-CARNIFEX - IN-VITRO STUDIES
A. Gobbetti et M. Zerani, ANDROGEN SYNTHESIS MODULATION BY PROSTAGLANDIN-E2 IS DIFFERENTIALLY MEDIATED VIA ADENYLATE-CYCLASE AND PHOSPHOLIPASE-C IN THE TESTIS OF THECRESTED NEWT, TRITURUS-CARNIFEX - IN-VITRO STUDIES, Biochemical and biophysical research communications, 211(3), 1995, pp. 1047-1052
To study the possible postreceptor mechanisms of prostaglandin E2 in m
odulating the male newt Triturus carnifex androgen synthesis, during r
eproduction, testes were in vitro superfused with medium alone, prosta
glandin E2, protein kinase C activator (phorbol-12-myristate-13-acetat
e), 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), pros
taglandin E2 plus AC inhibitor (2-0-methyladenosine), prostaglandin E2
plus protein kinase A inhibitor (H-89). In January (reproduction begi
nning), prostaglandin E2 and phorbol-12-myristate-13-acetate increased
androgens, while staurosporine and compound 48/80 counteracted the pr
ostaglandin E2 effect. In March (reproduction ending), prostaglandin E
2, dibutyryl cAMP and forskolin decreased androgens, while 2-0-methyla
denosine and H-89 counteracted the prostaglandin E2 effect. These data
suggest that in Triturus carnifex prostaglandin E2 increases testicul
ar androgens synthesis via phospholipase C at reproduction beginning;
on the contrary, this prostaglandin decreases androgens via adenylate
cyclase at reproduction ending. (C) 1995 Academic Press, Inc.