Aquatic ecosystems face ever increasing threats from pollutants, including those derived from exposure to bisphenol compounds (BPs). Bisphenols are endocrine disruptors with significant neurotoxic effects. This review examines the neurobehavioural impacts of bisphenol A (BPA) and its analogues (e.g. BPS, BPF, BPAF, and others) in zebrafish (Danio rerio), a widely used model organism in environmental and regulatory toxicology. Behavioural endpoints such as locomotor activity, anxiety, shoaling, and cognitive functions can be measured in zebrafish, providing insight into the potential neurotoxicity of chemicals. Bisphenols disrupt neural processes through mechanisms involving oxidative stress, endocrine disruption, neurotransmitter dysfunction, and altered gene expression related to neurodevelopment. Specific behavioural disruptions include impaired locomotor activity, heightened anxiety, altered social behaviours, and visual disturbances, often linked to structural damage in the nervous system. While BPA remains the most studied compound, evidence suggests other BPA analogues may have comparable or greater neurobehavioural toxicity. Implicated mechanisms underlying bisphenol-mediated behavioural events in zebrafish include cortisol metabolism, antioxidant defence, serotoninergic receptor signaling, and glutamate receptor signaling, revealing complex interactions that require further investigation. In addition, emerging studies point to the transgenerational effects of these compounds on neurobehavioural functions, necessitating further exploration of behaviour. This comprehensive review underscores the need for expanded research into the molecular pathways underlying BPs-induced neurotoxicity to help formulate better mitigation strategies and regulatory policies.
Keywords: Behaviour; Bisphenol; Endocrine disrupting compounds; Neurobehaviour; Zebrafish.
Copyright © 2025. Published by Elsevier Inc.