Meeting Abstract
Male reproductive abnormalities including altered testis function are becoming more common, and have been associated with fetal exposure to anti-androgenic endocrine disrupting chemicals (EDCs). These EDCs can disrupt the binding of hormones to their receptor, and alter testis morphology and function. Although limiting exposure to anti-androgens during pregnancy is the most efficient way to reduce fetal exposure to these chemicals, we are often exposed via unknown routes and are unable to adequately control our intake. Phase II detoxifying enzymes conjugate specific substances onto toxins to render them less harmful. Sulforaphane, is an inducer for GST (a phase II-inducing enzyme) and is expected to decrease the toxicity of EDCs reducing their effects on the developing fetus. We tested the hypothesis that sulforaphane can decrease the toxicity of the model anti-androgen vinclozolin on testis morphology and function. To test this hypothesis, we treated pregnant mice from embryonic day (E) 13.5- 16.5 with corn oil vehical alone, or vinclozolin (125 mg/kg) and supplemented vinclozolin exposed dams with 0, 15, 30, and 60 mg/kg of sulforaphane. Testes were dissected at E18.5 and processed for histology. Leydig, sertoli, and germ cell counts, and androgen concentration will be presented. The preliminary data suggests that Leydig cells increase with increasing sulforaphane supplementation supporting the hypothesis that testis cell function is rescued by increased Phase II detoxifying enzymes. Further data and their implications will be discussed.
