Human beings are routinely exposed to chronic and low dose of Bisphenols (BPs) due to their widely pervasiveness in the environment. BPs hold similar chemical structures to 17β-estradiol (E2) and thyroid hormone, thus posing threats to human health by rendering the endocrine system dysfunctional. Among BPs, Bisphenol-A (BPA) is the best-known and extensively studied endocrine disrupting compound (EDC). BPA possesses multisystem toxicity, including reproductive toxicity, neurotoxicity, hepatoxicity and nephrotoxicity. Particularly, the central nervous system (CNS), especially the developing one, is vulnerable to BPA exposure. This review describes our current knowledge of BPA toxicity and the related molecular mechanisms, with an emphasis on the role of Wnt signaling in the related processes. We also discuss the role of oxidative stress, endocrine signaling and epigenetics in the regulation of Wnt signaling by BPA exposure. In summary, dysfunction of Wnt signaling plays a key role in BPA toxicity and thus can be a potential target to alleviate EDCs induced damage to organisms.
Keywords: BPA exposure; Endocrine disrupting compound; Epigenetic; Oxidative stress; Wnt signaling.
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