Meeting Abstract
It is well established that embryos are particularly sensitive to alterations of their phenotype when exposed to chemicals during development (i.e. “fragile fetus”). These chemicals can be endogenous substances such as steroids produced by mothers or exogenous substances such as industrial chemicals present in the environment. Relative to what we know about how adult vertebrates modulate their exposure to steroids and environmental chemicals, we know remarkably little about how vertebrate embryos modulate exposure to these substances, despite their increased sensitivity. We have recently demonstrated that embryos are capable of modulating their exposure to maternal estradiol via steroid metabolism in the red-eared slider (Trachemys scripta). Importantly, this modulation can be inhibited by a common environmental chemical, bisphenol-A (BPA), which results in elevated estradiol within the egg during development. In this study, we examined the fate of BPA itself during embryonic development and found that BPA is also rapidly metabolized in red-eared slider eggs. Pairing these data with the previous findings that BPA inhibits estradiol metabolism, we are able to demonstrate that environmental chemicals can still elicit biological effects despite being rapidly metabolized. These findings highlight the dynamic nature of embryonic exposure to chemicals where an important effect of exogenous chemicals may simply be to alter exposure to endogenous chemicals. Going forward, it is critical that we understand how chemical exposure is realized by the embryo in order to predict how organisms may respond to changes in chemical exposure, and urge caution against viewing embryos as passive recipients of chemical signals during development.
