Meeting Abstract
Introduction of synthetic contaminants to ecosystems challenges organisms to respond to novel pollutants. 17α-ethinylestradiol (EE2) is an endocrine disrupting compound frequently found in wastewater effluent. Even trace concentrations of EE2 can induce significant phenotypic and physiological changes in fish. In wild populations, exposure to EE2 is unlikely to be confined to a single life history stage or generation. We were interested in determining the effects of compound (EE2, nonylphenol, mix) and route of exposure (water, diet, mix) on phenotypic development in juvenile mangrove rivulus (Kryptolebias marmoratus). We found that EE2 elicited higher liver vitellogenin (yolk protein) expression than unexposed controls, independent of route. EE2 administered through the diet resulted in fish with smaller gonads and body mass, and larger liver mass. These results suggest that EE2 has greater effects when fish are exposed through their diet than through the water, but that exposure through any route may impair reproductive function. This prompted a study of whether the environment experienced by a mother would impact offspring responses to exposure. We hypothesized that EE2 administration – via maternal exposure only, juvenile exposure only, or both – would impair growth and development compared to unexposed controls. We also hypothesized that the extent to which such impairments manifest will depend on whether juvenile and maternal exposure regimes match or mismatch. Offspring of exposed and unexposed fish were randomly assigned to an exposure environment that either matched or mismatched their mother’s. Growth, behavior, liver vitellogenin and gonad steroid receptor gene expression, and reproductive development were quantified. Here we present preliminary findings of that work.
