Meeting Abstract
Studies have shown that disorders associated with testicular dysgenesis syndrome (TDS) like hypospadias (mis-localized urethra) are increasing in prevalence, which is likely due to the increased use of endocrine-disrupting chemicals. Fetal Leydig cells are interstitial cells within the testes that are the primary source of androgens, and therefore play an important role in the development of the genitalia. However, the link between altered fetal Leydig cell function and altered genitalia development is unclear. To begin to understand the coordination between testis form and function and genital form and function we conducted a dose response experiment with the model anti-androgen vinclozolin that is known to induce hypospadias and measured morphological endpoints within the testes. We hypothesize that fetal Leydig cells will be hypertrophic and hypermorphic and that germ cells, seminiferous tubules, and Sertoli cells will show dose dependent effects. To test this hypothesis we exposed pregnant dams (N=3) at embryonic days (E) 13.5-16.5 to either a corn oil control (0), 100, 125, or 150 (mg/kg). Histological samples of the testes at E 18.5 were sectioned at 10μm and examined for morphological changes. Our findings will begin to characterize the link between fetal testis function and genitalia development. Understanding how endocrine-disrupting chemicals break the linkages between these organs could lead to advances in the treatment and prevention of testicular digenesis syndrome.
