an economically important wild fish species in China, has declined significantly in recent years. Bisphenol A (BPA) is an endocrine disrupting contaminant (EDC) that is ubiquitous in aquatic environments. It interferes with the growth, development, and reproduction of aquatic animals. Under normal conditions, sexual differentiation and reproductive development are controlled by sex hormones (estrogens and androgens) in fish. When present, EDCs upset the balance of hormones in the body and disrupt sexual differentiation. The effects of EDCs vary depending on the timing of exposure. Exposure during the embryo or juvenile stages can affect sexual differentiation and sex organ development. Conversely, exposure during the adult stages interferes with the organs or organ structure. We evaluated the effect of exposure to BPA (0, 50 μg/L, 200 μg/L, or 1 000 μg/L) in larvae (25 days post hatching; dph) and juveniles (95 dph) for 3 weeks and 2 weeks, respectively. We used fluorescent quantitative PCR (QRT-PCR) to quantify the level of gene expression in the gonads. BPA exposure significantly up-regulated the expression of expression, and down-regulated CYP17a, and mRNA was first down-regulated and then up-regulated, relative to the control, following a change in expression. The effects in the ovary were more complex; BPA initially inhibited the expression of , but expression later increased significantly. BPA inhibited the expression of in the ovary. These data suggest that BPA exposure interfered with steroid synthesis in the early stages of sexual differentiation in was up-regulated, thereby increasing steroid synthesis and altering the balance of estrogens and androgens. This change has an effect on sexual differentiation by interfering with the expression of T. obscurus by inhibiting steroidgenic gene expression, but there is a compensatory effect over time. Gene expression fluctuates in females, but the mechanism is currently poorly understood.