Abstract
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.
Highlights
The general consensus in the applied research community is that maternal stress adversely affects reproduction in vertebrates [1,2,3,4]
The effect of cortisol on the in vitro basal secretion of 17β-estradiol (E2) by ovarian follicles incubated in the presence of testosterone (T) Testosterone was added to the medium to determine if cortisol acted at the level of the aromatization of T to E2 by granulosal cells
The present study uses isolated fish ovarian follicles incubated in vitro to identify possible sites of direct action of cortisol on ovarian steroidogenesis; these in vitro studies eliminated many of the factors, such as actions on the hypothalamus-pituitary gland-ovary (HPO) axis, that may be involved in the responses to cortisol in vivo
Summary
The general consensus in the applied research community is that maternal stress adversely affects reproduction in vertebrates [1,2,3,4]. Despite extensive research over the last several decades, the mechanisms of action of stressors and “stress hormones” such as cortisol on reproductive functions have not been well-defined. This is probably because there is no single site of action of glucocorticoids on reproductive function. There are multiple sites of interaction of stress-related hormones on the maternal hypothalamus-pituitary gland-ovary (HPO) axis, as well as extensive metabolic outcomes, in addition to direct action on gonad function itself that have significant consequences for the development and maturation of gametes. Elevated ovarian glucocorticoids were found to have adverse affects on the maturation of oocytes and increased anovulation [13,14,15,16,17], but it is not clear whether these responses can be attributed to a direct action of the glucocorticoids on ovarian steroidogenesis
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