Meeting Abstract
Developing ovarian follicles are a primary site for steroid production in vertebrates and result in eggs that contain numerous maternally derived steroids. Embryonic exposure to these maternal steroids can have long-lasting consequences for the developing embryo, but recent work demonstrates that embryonic exposure to these steroids is modulated by steroid metabolism. Research to date suggests that little to no maternal steroids reach the embryo without first being metabolized. Currently we know very little about when and where this in ovo metabolism takes place. Additionally, the metabolism of maternal estradiol is inhibited by the endocrine disruptor bisphenol-A (BPA), altering embryonic exposure to this maternal steroid. In this study, we examined the potential for BPA to affect the in ovo metabolism of progesterone, testosterone, estrone, and corticosterone during the first 72 hours of development in the red-eared slider turtle (Trachemys scripta). We report that all four steroids are extensively metabolized within 24 hours of topical administration, but that BPA only inhibited the metabolism of estrone, while the metabolism of progesterone, testosterone, and corticosterone were not affected. The rapid metabolism of these steroids at such an early stage of embryonic development suggests that maternally derived enzymes are present in the egg at oviposition. The apparently unique susceptibility of estrogen metabolism to disruption by BPA may help explain the estrogenic effects of BPA and other so-called estrogenic endocrine disruptors. Deciphering the processes that underlie how embryos are exposed to maternal steroids will advance our understanding of how both maternal steroids and endocrine disruptors produce long-term phenotypic effects.
