Effects of Bisphenols on Testicular Steroidogenesis

• Main Authors: Federica Barbagallo, Rosita A. Condorelli, Laura M. Mongioì, Rossella Cannarella, Antonio Aversa, Aldo E. Calogero, Sandro La Vignera
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2020-06-01
• Series: Frontiers in Endocrinology
• Subjects: bisphenols; BPA; endocrine disruptors; testicular steroidogenesis; spermatogenesis
• Online Access: https://www.frontiersin.org/article/10.3389/fendo.2020.00373/full

Over the last decades, the adverse effects of human exposure to the so-called “endocrine disruptors” have been a matter of scientific debate and public attention. Bisphenols are synthetic chemicals, widely used in the manufacture of hard plastic products. Bisphenol A (BPA) is one of the best-known environmental toxicants proven to alter the reproductive function in men and to cause other health problems. Consumer concern resulted in “BPA free” products and in the development of bisphenol analogs (BPA-A) to replace BPA in many applications. However, these other bisphenol derivatives seem to have effects similar to those of BPA. Although a number of reviews have summarized the effects of BPA on human reproduction, the purpose of this article is to review the effects of bisphenols on testicular steroidogenesis and to explore their mechanisms of action. Testicular steroidogenesis is a fine-regulated process, and its main product, testosterone (T), has a crucial role in fetal development and maturation and in adulthood for the maintenance of secondary sexual function and spermatogenesis. Contradictory outcomes of both human and animal studies on the effects of BPA on steroid hormone levels may be related to various factors that include study design, dosage of BPA used in in vitro studies, timing and route of exposure, and other confounding factors. We described the main possible molecular target of bisphenols on this complex pathway. We report that Leydig cells (LCs), the steroidogenic testicular component, are highly sensitive to BPA and several mechanisms concur to the functional impairment of these cells.