LAUSR

In this study, the influence of bisphenol F (BPF) toward central neural system (CNS) was assessed using zebrafish embryos. We found that BPF could induce significant neurotoxicity towards zebrafish embryos, including inhibited locomotion, reduced moving distance and CNS cell apoptosis at an effective concentration of 0.0005 mg/L. Immunofluorescence assay showed that both microglia and astrocyte in zebrafish brain were significantly activated by BPF, indicating the existence of neuroinflammatory response. A motor neuron green fluorescence (MnGF) transgenic zebrafish assay showed that BPF significantly inhibited motor neuron development at 72 hpf. RNA-seq data indicated that neuronal developmental processes and cell apoptosis pathways were significantly affected by BPF exposure, which was consistent with the phenotypic results. Chip-Seq assay implied that the transcriptional changes were not mediated by ERα. Additionally, no significant change was found in neurotransmitter levels (5-hydroxytryptamine, dopamine, acetylcholine) or acetylcholinesterase (ache) enzyme activity after BPF exposure, indicating BPF may not affect neurotransmission. In conclusion, BPF could lead to abnormal neural outcomes during zebrafish early life stage through inducing neuroinflammation and CNS cell apoptosis even at environmentally relevant concentrations.