In this study, the influence of bisphenol F (BPF) toward central nervous system (CNS) was assessed using zebrafish embryos. We found that BPF could induce significant neurotoxicity toward 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. Peripheral motor neuron development was significantly inhibited by BPF 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, and acetylcholine) or acetylcholinesterase (Ache) enzyme activity after BPF exposure, indicating that 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 concentration.

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The COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is raging across the world, leading to a mortality rate of 3.4%. As a potential vaccine and therapeutic target, the nucleocapsid protein of SARS-CoV-2 (nCoVN) functions in packaging the viral genome and viral self-assembly. To investigate the biological effect of nCoVN to human induced pluripotent stem cells (iPSC), genetically engineered iPSC overexpressing nCoVN (iPSC-nCoVN) were generated by lentiviral expression systems. Unexpectedly, the morphology and proliferation rate of iPSC were changed after nCoVN expressing for two weeks. The pluripotency markers SSEA4 and TRA-1-81 were not detectable in iPSC-nCoVN. Meanwhile, iPSC-nCoVN lost the ability for differentiation into cardiomyocytes when using a routine differentiation protocol. Our data suggested that nCoVN disrupted the pluripotent properties of iPSC and turned them into fibroblasts, which provided a new insight to the pathogenic mechanism of SARS-CoV-2.