Abstract

Bisphenol B (BPB) exhibited higher estrogenic activity and anti-androgenic effects than bisphenol A (BPA) in vitro assays. This result indicates that BPB has higher priority for entry into expensive and stressful testing on animals. However, the disrupting mechanisms of BPB on steroid hormone signaling pathway by in vivo assay have not been investigated yet. In this study, the potential disrupting mechanisms of BPB on the hypothalamic–pituitary–gonadal (HPG) axis and liver were probed by employing the Organization for Economic Co-operation and Development (OECD) 21-day short-term fecundity assay with zebrafish. We found that BPB exposure (1 mg/L) could impair the reproductive function of zebrafish and decline the egg numbers, hatching rate, and survival rate. This finding is related to modifications of the testis and ovary histology of the treated zebrafish. The homogenate T levels in male zebrafish decreased in a concentration-dependent manner, and the E2 level significantly increased when exposed to 0.01, 0.1, and 1 mg/L BPB. Real-time polymerase chain reaction (PCR) was performed to examine the gene expressions in the HPG axis and liver. Hepatic vitellogenin (vtg) expression was upregulated in all exposure males, suggesting that BPB possesses estrogenic activity. The disturbed hormone balance was contributed by the significant alteration of the genes along the HPG axis. These alterations suggest that BPB can lead to adverse effects on the endocrine system of teleost fish, and these effects were more prominent in males than in females.

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