Chapter 1. Classical and Non-classical Estrogen Receptor Effects of Bisphenol A
Manoj Sonavane
Abstract
Bisphenol A (BPA) is an organic synthetic compound that widely serves as a monomer in the manufacturing of polycarbonate plastic and epoxy resins, used in the packaging of food and drinks, thermal paper, medical devices, and dental materials. BPA exposure has been associated with serious endocrine-disrupting effects in humans and wildlife. Due to its hormone-like properties, BPA can bind to estrogen receptors (ERs), thereby affecting body weight, cardiovascular functions, reproductive abnormalities, and tumorigenesis. Traditionally, BPA has been considered a weak estrogen compared to 17-β estradiol (E2) due to its low binding affinity and transcriptional activity after ER activation. However, BPA could elicit a different endocrine-disrupting capacity at very low concentrations with the same or even higher efficiency than E2. Furthermore, BPA effects rely on several non-classical ER pathways, such as interaction with a membrane ER that triggers rapid estrogenic signaling via the activation of cellular kinase systems (non-genomic) and induction of several nuclear transcription factors (genomic). Thus, considering the incidence and prevalence of health problems associated with increased endocrine disruption worldwide, the purpose of the chapter is to analyze with substantiated scientific evidence the strong estrogenic activity of BPA when it acts through classical and non-classical ER triggered pathways.