The mechanisms underlying the developmental effects of bisphenol F on zebrafish.

With the increasing use of bisphenol F (BPF) as BPA alternative, BPF are widely distributed in multiple environment media. Our previous study demonstrated that BPF possess equivalent toxicity towards zebrafish as BPA, while its toxic mechanism remains largely unknown. To investigate the mechanisms mediating the developmental effects of BPF, zebrafish embryos were exposed to 0.0005, 0.5, and 5.0 mg/L BPF. Morphological examination indicated that BPF exposure led to depigmentation, decreased heart rate, inhibited spontaneous movement, hatch inhibition, and spinal deformation. Motor neuron-green fluorescence zebrafish assay indicated that exposure to 0.5 or 5.0 mg/L BPF affected embryonic motor neuron development, which is consistent with the spinal defect and spontaneous movement inhibition. Transcriptomic analysis showed that genes associated with the observed symptoms, including neuron development (ngln2a, socs3a, fosb), cardiac development (klf2a), and spinal deformation (ngs, col8a1a, egr2a), were down-regulated after exposure to either 0.0005 (environmental relevant concentration) or 0.5 mg/L BPF. This partially explained the mechanisms underlying the effects of BPF. In conclusion, BPF had the potential to affect zebrafish development even at environmental level through down-regulating associated genes.

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