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 mu g/L) until 144 hpf. The results showed that 100 and 1000 mu g/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, thr alpha, thr beta 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, alpha-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.

Automated summary

The study found that exposure to BPB in zebrafish larvae led to abnormal thyroid hormone levels and inhibited neuronal development, potentially causing neurotoxicity and thyroid disruption.