Developmental bisphenol A exposure modifies gene expression without altering stress or cognitive outcomes in offspring of a live-bearing fish.

Endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), are prevalent pollutants in aquatic ecosystems and may present developmental risks to exposed organisms, especially in viviparous matrotrophic organisms, where the physiological processes that enable mothers to supply nutrients to embryos during gestation (matrotrophy) also allow EDCs to reach the developing offspring. In this study we examined the impact of prenatal BPA exposure in the live-bearing fish, Heterandria formosa. Gravid females were exposed to 200 μg/L BPA dissolved in ethanol, water control, or ethanol solvent to measure direct maternal effects via changes in cortisol and indirect effects of exposure on offspring cortisol. Additionally, we evaluated offspring behavior and cognitive performance along with gene expression after the exposure ceased. We predicted indirect effects of exposure to BPA on offspring, but contrary to our predictions, prenatal BPA exposure did not significantly affect offspring cognition, behavior, cortisol, or overall gene expression. However, in exploratory comparisons of solving status we found evidence that BPA and ethanol dampened the gene expression differences between solvers and non-solvers that were present under baseline (water). These results suggest that while BPA alters gene expression patterns under certain conditions, behavioral and cognitive traits, such as problem-solving and inhibitory control, are likely regulated by factors beyond gene expression alone, including physiological processes like cortisol regulation and potentially gene networks. Moreover, our results suggest this species of live-bearing fish provides protection for offspring from long-term effects of high prenatal BPA exposure, although the possibility of epigenetic or delayed multigenerational effects cannot be ruled out.