Stimulation in vitro of estradiol secretion by the ovary of a cichlid fish, Sarotherodon aureus.

The objective of the present study was to investigate the nature of the gonadotrophic stimulation of estradiol (E2) secretion by the ovary of a teleost fish in vitro. Spontaneous output of E2 decreased to a low baseline after 3 hr of superfusion and increased to a maximal level 2-3 hr after the introduction of homologous pituitary extract (T-PE) or human chorionic gonadotrophin into the superfusion system. Addition of the phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX, 0.5 mM), into a closed-system incubation resulted in an augmented response of the ovary to either dibutyryl cyclic AMP or to T-PE. It is concluded that the gonadotrophic stimulation of E2 secretion from the ovary of Sarotherodon aureus is mediated by cyclic AMP as a second messenger. Purified carp GTH or ovine LH stimulated E2 secretion in vitro in a dose-dependent manner in the range 3-300 ng/ml. In order to examine the effect of ovarian stage on E2 secretion rate in response to a gonadotrophic stimulation, fish with regressed ovaries were transferred to 30 degrees for 29 days. Five fish were bled every 4 days and their ovaries were incubated individually with and without T-PE. A sevenfold increase in plasma E2 occurred 4 days after the transfer to 30 degrees, whereas the first significant increase in the gonadosomatic index (GSI) could be noted only on Day 12. Both the spontaneous secretion rate of E2 in vitro (E2 basal) and the secretion rate in response to T-PE (E2 max) increased together with the GSI throughout the experiment. However, the ratio E2 max/E2 basal, which reflects the capacity of the ovary to respond to the gonadotrophic stimulation, reached a peak on Day 16, when GSI was about 1. The ratio then declined and remained low until the end of the experiment. The early increase in plasma E2 can be explained by the elevated sensitivity of the ovary to GTH during the initial phase of the temperature-induced ovarian recrudescence. The high level of plasma E2 maintained from Day 16 on may be due to a spontaneous synthesis and secretion of the steroid, not necessarily controlled by GTH.