Regulation of Leydig Cell Differentiated Function by the Industrial Chemical

Exposure of the population to bisphenol A (BPA) is significant due to its extensive use in the manufacture of a wide variety of consumer products, including polycarbonate plastics and epoxy resins. However, there is concern that early-life exposure to BPA may alter developmental programming and predispose individuals to adverse health outcomes such as infertility and obesity in later life. This dissertation describes the adverse effects of early-life exposure to BPA on Leydig cell function using the rat model. Testicular Leydig cells are the predominant source of the male sex steroid hormone testosterone, which supports the male phenotype. The objectives were to investigate the effects of developmental BPA exposure on (i) Leydig cell development; (ii) adipose tissue derived molecules (e.g., adiponectin) and their regulation of Leydig cells; and, (iii) estrogen metabolism and antioxidant capacity in Leydig cells. Exposure of male rats to BPA by maternal gavage at doses of 2.5 and 2