Endocrine Control of Oocyte Maturation

Periovulatory changes in catfish ovarian oestradiol-17beta, oestrogen-2-hydroxylase and catechol-O-methyltransferase during GnRH analogue-induced ovulation and in vitro induction of oocyte maturation by catecholoestrogens

“…The patterns of periovulatory changes in OE 2 and CE-related enzymes strongly indicate enhanced OE 2 catabolism towards CE formation and degradation in the catfish ovary. Since oestrogens have little or even an inhibitory role on oocyte final (meiotic) maturation in teleosts including the catfish (Sundararaj & Goswami 1977, Nagahama 1987, their removal by converting into CE may be an important physiological step during the periovulatory period. A direct demonstration of CEs and their metabolites remains.…”

“…When the oocytes were pre-incubated with cyanoketone and epostane (inhibitors of 3 -hydroxysteroid dehydrogenase, 3 -HSD), and aminoglutethimide (a P450 antagonist) for 2 h, and then stimulated with different CEs for 8 h, and subsequently incubated again with steroidogenic inhibitors, the GVBD response was not affected, indicating that it was independent of de novo steroidogenesis by ovarian follicles. It has been demonstrated that the 3 -HSD blockers cyanoketone and epostane do not block progesterone-or 17 ,20 -DP-induced oocyte maturation but block gonadotrophin/pituitary extract-induced maturation in teleosts, including catfish (Nagahama 1987, Rao & Haider 1992. In the present study, we also used the P450 antagonist, aminoglutethimide, that has a broad action at several steroid conversion steps and obtained similar results.…”

“…The strong inhibitory response of actinomycin D on CE-induced GVBD response is similar to that observed in gonadotrophininduced GVBD but different from other steroid-(e.g. deoxycorticosterone, 17 ,20 -DP) and insulin-like growth factor-I-induced oocyte maturation (Sundararaj & Goswami 1977, Goetz 1983, Nagahama 1987, Jalabert et al 1991. In the latter case, only translational activity (protein synthesis) was involved during the GVBD response.…”

“…The sequential physiological events of vitellogenesis, oocyte final maturation and ovulation during fish oogenesis are under the differential control of regulatory mechanisms involving principally the pituitary gonadotrophin and ovarian steroid regulators (Chieffi & Pierantoni 1987, Ho 1987, Nagahama 1987, Yoshikuni & Nagahama 1991, Kagawa 1994. The vitellogenic phase is initiated and maintained by one of the gonadotrophins (gonadotrophin-I (GTH-I) or follicle-stimulating hormone (FSH)) in the two gonadotrophin model species (Kawauchi et al 1989, Yoshikuni & Nagahama 1991, Swanson & Dittman 1997 through the mediation of ovarian oestrogens, principally oestradiol-17 (OE 2 ).…”

“…The vitellogenic phase is initiated and maintained by one of the gonadotrophins (gonadotrophin-I (GTH-I) or follicle-stimulating hormone (FSH)) in the two gonadotrophin model species (Kawauchi et al 1989, Yoshikuni & Nagahama 1991, Swanson & Dittman 1997 through the mediation of ovarian oestrogens, principally oestradiol-17 (OE 2 ). Oocyte maturational and ovulatory events are initiated by the other gonadotrophin (gonadotrophin-II (GTH-II) or luteinizing hormone (LH)) through the mediation of a maturation-inducing hormone or substance (MIH or MIS), the most common being an ovarian progesterone derivative, 17 , as in many salmonids, cyprinids and silurids, or 17 ,20 ,20 , as in sciaenid fish (Goetz 1983, Nagahama 1987, Scott & Canario 1987, Thomas 1994. MIS activity was also demonstrated for corticosteroids (deoxycorticosterone and cortisol) in several teleosts including catfish (Goswami & Sundararaj 1974, Sundararaj & Goswami 1977, Goetz 1983, Upadhyaya & Haider 1986, Rao & Haider 1992, Haider 1997.…”