Adverse effects of bisphenol B exposure on the thyroid and nervous system in early life stages of zebrafish

Bisphenol B (BPB), a widely used alternative of bisphenol A (BPA), has been detected in various environmental media and foodstuffs. However, the knowledge of the health risks about BPB is still limited. In this study, the effects of BPB on thyroid hormone homeostasis and neuronal development were evaluated by exposure of embryos 2 h post-fertilization (hpf) to BPB (0, 1, 10, 100 and 1000 μg/L) until 144 hpf. The results showed that 100 and 1000 μg/L BPB exposed larvae exhibited abnormal morphologies in phenotype and brain histological patterns. Significant decline of thyroid hormone thyroxine (T4) content and elevation of 3,5,3′-triiodothyronine (T3) content, along with the up-regulated expression of tg, trhr1, dio1, dio2, thrα, thrβ genes and down-regulated expression of tsh, ttr and trh genes in BPB exposed zebrafish larvae were observed. Moreover, locomotor activity of larvae was decreased, and the transcription of genes (e.g., elavl3, gap43, zn5, α-tubulin, syn2a and mbp) related to neuronal development were inhibited after exposure to BPB. The mechanism of neurotoxicity and thyroid disruption in zebrafish larvae induced by BPB were discussed. [Display omitted] •BPB induced thyroid disruption through inhibiting T4 and increasing T3 levels in zebrafish larvae.•Genes involved in HPT axis were remarkably modulated after BPB exposure.•Genes related to neuronal development altered significantly after BPB exposure.•BPB induced developmental and neuronal toxicity in zebrafish larvae.