Impact of Bisphenol A on Structure and Function of Mitochondria: A Critical Review

Abstract

Bisphenol A (BPA) is an industrial chemical used extensively to manufacture polycarbonate plastics and epoxy resins. Because of its estrogen-mimicking properties, BPA acts as an endocrine-disrupting chemical. It has gained attention due to its high chances of daily and constant human exposure, bioaccumulation, and the ability to cause cellular toxicities and diseases at extremely low doses. Several elegant studies have shown that BPA can exert cellular toxicities by interfering with the structure and function of mitochondria, leading to mitochondrial dysfunction. Exposure to BPA results in oxidative stress and alterations in mitochondrial DNA (mtDNA), mitochondrial biogenesis, bioenergetics, mitochondrial membrane potential (MMP) decline, mitophagy, and apoptosis. Accumulation of reactive oxygen species (ROS) in conjunction with oxidative damage may be responsible for causing BPA-mediated cellular toxicity. Thus, several reports have suggested using antioxidant treatment to mitigate the toxicological effects of BPA. The present literature review emphasizes the adverse effects of BPA on mitochondria, with a comprehensive note on the molecular aspects of the structural and functional alterations in mitochondria in response to BPA exposure. The review also confers the possible approaches to alleviate BPA-mediated oxidative damage and the existing knowledge gaps in this emerging area of research.

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