Oocyte maturation in the amago salmon (Oncorhynchus rhodurus): in vitro effects of salmon gonadotropin, steroids, and cyanoketone (an inhibitor of 3 beta-hydroxy-delta 5-steroid dehydrogenase).
The effect of partially purified chinook salmon gonadotropin (SG-G100) and a number of steroids on the induction of germinal vesicle breakdown (GVBD) in amago salmon (Oncorhynchus rhodurus) oocytes (with intact follicle layers) was investigated in vitro. SG-G100 was effective only at the highest concentration tested (1 microgram/ml). 17 alpha,20 beta-Dihydroxy-4-pregnen-3-one (17 alpha,20 beta-diOHprog) was the most potent maturation-inducing steroid tested, followed by 17 alpha-hydroxyprogesterone. Testosterone or deoxycorticosterone (DOC) enhanced the rate of GVBD in response to SG-G100. DOC also enhanced the response to 17 alpha,20 beta-diOHprog but testosterone was without effect, suggesting that DOC has a direct action on the oocyte while testosterone probably acts at the level of the follicle. Estradiol-17 beta had no effect on GVBD in response to SG-G100 or 17 alpha,20 beta-diOHprog. The action of SG-G100 was shown to be dependent on the synthesis of a second delta 4 steroidal mediator of maturation since cyanoketone, a specific inhibitor of 3 beta-hydroxy-delta 5-steroid dehydrogenase, completely abolished the maturational effects of the gonadotropin and pregnenolone but not delta 4 steroids. Radioimmunoassay of media in which oocytes were induced to mature in vitro with SG-G100 revealed significantly elevated levels of progesterone and 17 alpha,20 beta-diOHprog. Estradiol-17 beta levels, high in control media, were only elevated twofold by SG-G100. Levels of the two progestogens were extremely low or nondetectable in media in which oocytes were incubated with cyanoketone, while estradiol-17 beta levels remained high. These results are discussed in relation to other evidence indicating that 17 alpha,20 beta-diOHprog is the naturally occurring maturation-inducing steroid of amago salmon. The role of other steroid hormones, particularly the possible involvement of corticosteroids, in the control of final oocyte maturation in teleosts is explored.
D019326:17-alpha-Hydroxyprogesterone; D015096:3-Hydroxysteroid Dehydrogenases / Q000037:antagonists & inhibitors; D000737:Androstenols / Q000494:pharmacology*; D000818:Animals; D003489:Cyanoketone / Q000494:pharmacology*; D003900:Desoxycorticosterone / Q000494:pharmacology; D004958:Estradiol / Q000096:biosynthesis; D005260:Female; D006062:Gonadotropins / Q000494:pharmacology*; D006908:Hydroxyprogesterones / Q000494:pharmacology; D066298:In Vitro Techniques; D009865:Oocytes / Q000187:drug effects* / Q000378:metabolism; D009866:Oogenesis / Q000187:drug effects; D010063:Ovum / Q000187:drug effects*; D011374:Progesterone / Q000096:biosynthesis; D012474:Salmon; D013256:Steroids / Q000494:pharmacology*; D013739:Testosterone / Q000494:pharmacology
D000737:Androstenols; D006062:Gonadotropins; D006908:Hydroxyprogesterones; D013256:Steroids; C016844:salmon gonadotropin; C021012:17 alpha,20 beta-dihydroxypregn-4-en-3-one; D013739:Testosterone; D003900:Desoxycorticosterone; D003489:Cyanoketone; D011374:Progesterone; D004958:Estradiol; D019326:17-alpha-Hydroxyprogesterone; D015096:3-Hydroxysteroid Dehydrogenases