Bisphenol A (BPA) is ubiquitous in the environment and poses a threat to wildlife and human health. It has been reported that BPA may cause the neurotoxicity during gestational and neonatal periods. Cyanidin-3-O-glucoside (C3G) is one of the most abundant anthocyanins that has shown multiple bio-functions. In this study, the protective effects and possible mechanism of C3G against BPA-induced neurodevelopment toxicity in zebrafish embryos/larvae were studied. The results showed that co-exposure of C3G (25 μg/mL) significantly attenuated BPA-induced deficit in locomotor behavior and restored the BPA-induced aberrant changes in brain morphology of zebrafish larvae. Further studies showed that the defects of central nervous development and the downregulated neurogenesis relative genes induced by BPA were significantly counteracted by co-exposure with 5 μg/mL of C3G. In addition, C3G (25 μg/mL) mitigated the decline of glutathione (GSH) content and enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT), attenuated oxidative stress and cell apoptosis induced by BPA in zebrafish. The enhancements of the expression of genes involved in the Nrf2-ARE pathway (Nrf2, HO-1, NQO1, GCLC, and GCLM) were also observed by co-exposure of C3G. The results indicate that C3G exerts protective effects on BPA-induced neurodevelopmental toxicity through improving transcription of neurogenesis related genes, enhancing antioxidative defense system and reducing cell apoptosis by regulation of apoptotic genes in zebrafish larvae. The results suggest that anthocyanins may play important role against the exogenous toxicity for vertebrates.
Keywords: Antioxidant; Bisphenol A; Cyanidin-3-O-glucoside; Neuroprotection; Zebrafish.
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