Steroid production by ovarian follicles of the viviparous guppy (Poecilia reticulata) and its regulation by precursor substrates, dibutyryl cAMP and forskolin.
Production in vitro of estradiol-17 beta, testosterone, 17 alpha-20 beta-dihydroxy-4-pregnen-3-one (17 alpha,20 beta-P), 17 alpha-hydroxyprogesterone, and progesterone by follicles of the guppy at various stages of oocyte growth and gestation was investigated. Basal production of estradiol-17 beta was highest in 0.8- and 1.2-mm follicles, whereas that of testosterone and 17 alpha,20 beta-P was highest in 1.6-mm (postvitellogenic) follicles. Levels of these steroids declined after fertilization and were undetectable in late gestation and postpartum follicles. 17 alpha-Hydroxyprogesterone and progesterone levels were low at all stages. Thus, none of these steroids appears to be involved in maintaining gestation. Regulation of estradiol-17 beta and 17 alpha,20 beta-P secretion by vitellogenic (1.0 mm) and postvitellogenic follicles by precursor substrates, dbcAMP (0.1 to 10 mM) and forskolin (1 to 100 microM), was also investigated. Vitellogenic follicles synthesized increased quantities of estradiol-17 beta in the presence of exogenous testosterone, whereas estradiol-17 beta production by postvitellogenic follicles was not altered by testosterone. These results suggest decreased aromatase activity in the postvitellogenic follicles. Dibutyryl cAMP and/or forskolin stimulated testosterone and estradiol-17 beta production by vitellogenic follicles but did not stimulate conversion of testosterone to estradiol-17 beta, suggesting that the adenylate cyclase system stimulates estradiol-17 beta production by stimulating testosterone production but does not mediate conversion of testosterone to estradiol-17 beta. Postvitellogenic follicles synthesized increased quantities of 17 alpha,20 beta-P in response to 17 alpha-hydroxyprogesterone in a dose-dependent manner. Although 1 microM of forskolin stimulated 17 alpha,20 beta-P production by postvitellogenic follicles in the absence of exogenous 17 alpha-hydroxyprogesterone, 100 microM of forskolin inhibited 17 alpha,20 beta-P production. Dibutyryl cAMP, however, did not affect 17 alpha,20 beta-P production. In the presence of 50 ng of 17 alpha-hydroxyprogesterone, dbcAMP (10 mM) and forskolin (1 to 100 microM) suppressed 17 alpha,20 beta-P production. It is suggested that cAMP mediates 17 alpha,20 beta-P production up to a certain threshold level, beyond which it inhibits 17 alpha,20 beta-P production.
Venkatesh
B
B
Department of Zoology, National University of Singapore.
Tan
C H
CH
Lam
T J
TJ
D019326:17-alpha-Hydroxyprogesterone; D000704:Analysis of Variance; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D005576:Colforsin / Q000494:pharmacology*; D046508:Culture Techniques; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000096:biosynthesis; D005260:Female; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis*; D006908:Hydroxyprogesterones / Q000378:metabolism; D009866:Oogenesis / Q000502:physiology; D006080:Ovarian Follicle / Q000187:drug effects* / Q000378:metabolism*; D011036:Poecilia / Q000502:physiology*; D049590:Postpartum Period / Q000378:metabolism; D011247:Pregnancy / Q000378:metabolism; D011374:Progesterone / Q000096:biosynthesis; D013739:Testosterone / Q000096:biosynthesis
D012739:Gonadal Steroid Hormones; D006908:Hydroxyprogesterones; C007433:17,20-dihydroxy-4-pregnen-3-one; D005576:Colforsin; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D003994:Bucladesine; D019326:17-alpha-Hydroxyprogesterone