Bisphenol F-Induced Neurotoxicity toward Zebrafish Embryos

Area of Science:

• Environmental toxicology
• Neuroscience
• Developmental biology

Background:

• Bisphenol A (BPA) is a known endocrine disruptor.
• Concerns exist regarding the safety of its analog, Bisphenol F (BPF).
• Understanding BPF's impact on the central nervous system (CNS) is crucial.

Purpose of the Study:

• To investigate the neurotoxic effects of Bisphenol F (BPF) on zebrafish embryos.
• To elucidate the mechanisms underlying BPF-induced neurotoxicity, including neuroinflammation and apoptosis.
• To assess the impact of BPF on neural development and neurotransmission.

Main Methods:

• Zebrafish embryos were exposed to varying concentrations of BPF.
• Locomotion, CNS cell apoptosis, and motor neuron development were assessed.
• Immunofluorescence, RNA-seq, and Chip-seq assays were employed to analyze molecular responses.
• Neurotransmitter levels and acetylcholinesterase activity were measured.

Main Results:

• BPF induced significant neurotoxicity, including inhibited locomotion and CNS cell apoptosis at 0.0005 mg/L.
• BPF exposure led to significant activation of microglia and astrocytes, indicating neuroinflammation.
• Peripheral motor neuron development was inhibited, and neuronal developmental pathways were affected.
• Transcriptional changes were not mediated by ERα, and neurotransmission was not significantly altered.

Conclusions:

• Bisphenol F causes neurodevelopmental abnormalities in zebrafish early life stages.
• Neuroinflammation and CNS cell apoptosis are key mechanisms of BPF neurotoxicity.
• BPF poses a risk to neural development even at environmentally relevant concentrations.