PNNL

Abstract

Transient developmental exposure to 0.1µM bisphenol A (BPA) results in larval zebrafish hyperactivity and learning impairments in the adult, while exposure to 80µM BPA results in teratogenic responses, including craniofacial abnormalities and edema. The mode of action underlying these effects is unclear. We used global gene expression analysis to identify candidate genes and signaling pathways that mediate BPA's developmental toxicity in zebrafish. Exposure concentrations were selected and anchored to the positive control, 17ß-estradiol (E2), based on previously determined behavioral or teratogenic phenotypes. Functional analysis of differentially expressed genes revealed distinct expression profiles at 24h post fertilization for 0.1µM versus 80µM BPA and 0.1µM versus 15µM E2 exposure, identification of prothrombin activation as a top canonical pathway impacted by both 0.1µM BPA and 0.1µM E2 exposure, and suppressed expression of several genes involved in nervous system development and function following 0.1µM BPA exposure.