Zeitschrift für Aquakulturforschung und -entwicklung

Abstrakt

Cortisol Inhibition of 17b-Estradiol Secretion by Rainbow Trout Ovarian Follicles Involves Modulation of Star and P450scc Gene Expression

S. Barkataki, N. Aluru, M. Li, L. Lin, H. Christie, M.M. Vijayan and J.F. Leatherland

Maternal stress associated with elevated maternal cortisol levels has well-demonstrated adverse affects on reproduction in vertebrates, including impaired ovarian steroidogenesis. Currently, the potential sites of action of cortisol on ovarian function are not known. Studies were carried out to examine the mechanism(s) by which cortisol suppresses steroidogenesis by mid-vitellogenic stage rainbow trout (Oncorhynchus mykiss) ovarian follicles. 17b-Estradiol and testosterone synthesis, and the expression of key steroidogenesis-related genes (using real time RT-PCR) were measured. Follicles were also incubated in the presence of several tritium-labelled steroids ([3H]17α-hydroxyprogesterone, [3H]testosterone, [3H]androstenedione), and the tritium-labeled steroid products were separated by reverse-phase HPLC to look for possible affects of cortisol on specific steroidogenic enzyme function. Cortisol inhibited 17b-estradiol and testosterone synthesis, but had no affect on the formation of tritium-labelled estrogens from any of the tritium-labeled substrates, suggesting that the suppressive action of the glucocorticoid did not operate by inhibiting estrogen synthesis from androgens. Conversely, in the presence of cortisol in the medium, the relative expression of genes encoding for steroidogenic acute regulatory (StAR) protein and P450 side chain cleavage (P450scc) enzyme was suppressed, suggesting that the cortisol inhibition of steroidogenesis is prior to the synthesis of progestogens, possibly inhibiting either the expression and/or turnover of the genes encoding for StAR and P450scc proteins. The study shows that maternal stress during the critical phase of follicle vitellogenesis will have deleterious effects on oocyte development and growth.