By Jamie Volk

Faculty Mentor: Dr. Dianne Baker

Abstract

Bisphenol A (BPA), a common component of polycarbonate plastics and epoxy resins, is a well-established endocrine-disrupting chemical (EDC) linked to adverse reproductive outcomes. In response to increasing regulatory restrictions, structurally similar analogs such as bisphenol B (BPB) have been introduced into consumer products, despite limited toxicological characterization. Emerging evidence suggests that these substitutes may retain endocrine-disrupting properties comparable to BPA, raising concerns about their safety. This study examined the effects of embryonic BPB exposure on male reproductive development using zebrafish (Danio rerio), a widely used vertebrate model for endocrine disruption research. I hypothesized that early-life exposure to BPB alters the expression of genes critical for sex differentiation and reproductive function. To test this, embryos were exposed to increasing concentrations of BPB during early development. Following exposure, transcript levels of key genes involved in gonadal development and endocrine regulation (dmrt1, cyp19a1b, dazl, nanos1, and fshb) were quantified using RT-qPCR. By focusing on this critical window of development, this study addresses key gaps in understanding the reproductive toxicity of BPB. These findings contribute to ongoing evaluation of BPA alternatives and highlight the need for further investigation into the safety of structurally similar endocrine-disrupting compounds in consumer products.