Does bisphenol A (BPA) participates in the pathogenesis of Polycystic Ovary Syndrome (PCOS)?

• Published in: Clinics (São Paulo, Brazil) Brazil), 2023-01, Vol.78, p.100310-100310, Article 100310
• Main Authors: Urbanetz, Lorena Ana Mercedes Lara, Junior, José Maria Soares, Maciel, Gustavo Arantes Rosa, Simões, Ricardo dos Santos, Baracat, Maria Cândida Pinheiro, Baracat, Edmund Chada
• Format: Article
• Language: English
• Subjects: Anovulation - complications; Bisphenol A; Endocrine disruptors; Female; Humans; Hyperandrogenism; Hyperandrogenism - complications; Infant, Newborn; Insulin resistance; MEDICINE, GENERAL & INTERNAL; Obesity; Phenols - toxicity; Polycystic Ovary Syndrome; Polycystic Ovary Syndrome - chemically induced; Pregnancy
• ISSN: 1807-5932; 1980-5322; 1980-5322
• DOI: 10.1016/j.clinsp.2023.100310

•Bisphenola A (BPA) is an endocrine disruptor widely investigated as a possible environmental contributor to the pathogenesis of Polycystic Ovary Syndrome (PCOS).•Due to its structural similarity with the Estrogen molecule (E2), it acts as a xenoestrogen, binding to genomic and non-genomic estrogen receptors, causing metabolic and hormonal changes that lead to PCOS (hyperandrogenism, insulin resistance, hyperinsulinemia, obesity, atherogenic dyslipidemia, anovulation, and ovarian cysts).•The aim and of this review were to present the mechanisms of bisphenol A participation in the pathogenesis of Polycystic Ovary Syndrome. PCOS is an endocrine disorder characterized by chronic anovulation, hyperandrogenism, and polycystic ovaries. Its etiology is uncertain. It is debated whether BPA would be a component of the environmental factor in the etiology of PCOS. Contamination by BPA can occur from food packaging (exposure during the diet) and through skin absorption and/or inhalation. It can be transferred to the fetus via the placenta or to the infant via breast milk, and it can be found in follicular fluid, fetal serum, and amniotic fluid. The phenolic structure of BPA allows it to interact with Estrogen Receptors (ERs) through genomic signaling, in which BPA binds to nuclear ERα or Erβ, or through nongenomic signaling by binding to membrane ERs, prompting a rapid and intense response. With daily and constant exposure, BPA's tendency to bioaccumulate and its ability to activate nongenomic signaling pathways can alter women's metabolic and reproductive function, leading to hyperandrogenism, insulin resistance, obesity, atherogenic dyslipidemia, chronic inflammatory state, and anovulation and favoring PCOS. The harmful changes caused by BPA can be passed on to future generations without the need for additional exposure because of epigenetic modifications. Not only high BPA levels can produce harmful effects, but at low levels, BPA may be harmful when exposure occurs during the most vulnerable periods, such as the fetal and neonatal periods, as well as during the prepubertal age causing an early accumulation of BPA in the body. Learning how BPA participates in the pathogenesis of PCOS poses a challenge and further studies should be conducted.