[No authors listed]
Bisphenol F (BPF) has become a predominant bisphenol contaminant in recent years. It has significant estrogenic properties in both in vivo and in vitro studies. We have previously studied the disrupting mechanisms of BPF on the hypothalamic-pituitary-gonadal axis of adult zebrafish. However, the effects of BPF exposure on development and sexual differentiation of zebrafish embryos/larvae remain unclear. To determine the effects of BPF on the critical stage of sex differentiation in zebrafish, zebrafish embryos/larvae were exposed to 1, 10, 100, and 1000â¯Î¼g/L BPF from fertilization to 60â¯days post-fertilization (dpf). Developmental malformations were induced by exposure to BPF from 2â¯h post-fertilization (hpf), with a LC50 of 10,030â¯Î¼g/L at 96â¯hpf and 9391â¯Î¼g/L at 120â¯hpf. Long-term exposure during sex differentiation tended to result in a female sex ratio bias. Histological analyses at 60â¯dpf indicated that the development of ovo-testes and immature ovaries was induced by 100 and 1000â¯Î¼g/L BPF. Homogenate testosterone levels decreased and 17β-estradiol levels increased in zebrafish in a concentration-dependent manner. BPF exposure suppressed gene expression of double sex, Mab3-related transcription factor 1(dmrt1), fushi tarazu factor 1d (ff1d), sry-box containing gene 9a (sox9a) and anti-Mullerian hormone (amh); induced expression of the forkhead box L2 transcription factor (foxl2), leading to increased expression of aromatase (cyp19a1a), which promoted production of estrogens, and further caused phenotypic feminization of zebrafish. These results suggest that developmental exposure to BPF has adverse effects on sexual differentiation, and the results were useful for a BPF risk assessment.
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