Chronic Bisphenol A Induced Neurotoxicity: Exposure Risk, Molecular Fate Within Carp and Its Potential Phytoremediation

Bisphenol A (BPA) is an endocrine-disrupting toxicant commonly used in the plastics industry, as a result, it is present in large quantities in the environment. Therefore, current study was designed to assess BPA induced neurotoxicity and molecular fate within common carp ( Cyprinus carpio), ), largely used edible fish. Following 6 weeks exposure to BPA 1/5th of 96 h LC50 50 (1.31 mg/L), brain exhibited oxidative damage, which was evidenced by compromised antioxidant system (CAT, SOD, GSH) and increased level of biomacromolecule peroxidation (MDA and 8-OHDG). Functional damage to the brain observed in the form of blood-brain barrier disruption (decreased tight junction gene expression) and nerve conduction impairment (reduced acetylcholinesterase activity). Mechanistically, apoptotic cell death indicated by characteristic alteration in key biomarkers (bcl-2, caspase, and p53-related gene family). Whereas, coadministration of powdered PP (pomegranate peel) (8 %) with BPA effectively mitigated the BPA toxicity, as evidenced by the restoration of the above-mentioned bioindicators. Thereby, BPA-induced neurotoxicity could be potentially detoxified by applying PP dietary enrichment.