Hypothyroidism induced with iopanoic acid and propylthiouracil fails to disrupt testicular function as determined by serum testosterone, spermatogenesis, and seminiferous tubule morphology

The role of the thyroid hormones, triiodothyronine and thyroxine, in the hormonal control of mammalian testicular function has not been clearly delineated. Previous data regarding the effects of hypothyroidism and hyperthyroidism on testicular function, specifically spermatogenesis, has provided only conflicting results; and it is equivocal whether hypothyroidism can effectively disrupt qualitative and quantitative spermatogenesis. To examine the effect of acute hypothyroidism on spermatogenesis, adult male rats were injected with either iopanoic acid (lOP) or propylthiouracil (PTU), two goitrogens with specific mechanisms of action, for four weeks. Controls were injected with propylene glycol. Weekly blood samples were analyzed for triiodothyronine, thyroxine and testosterone. At the end of the experimental period (5 weeks), testicular tissue was excised and seminiferous tubules were prepared for histological analysis. Serum assays of the thyroid hormones revealed that the treated animals had become hypothyroid. Analysis of serum testosterone concentrations revealed no differences among the groups. Light microscopy revealed no morphological changes of the seminiferous tubules or disruption of spermatogenesis in the lOP and PTU treated animals based on germ cell populations. These data suggest that acute hypothyroidism does not interfere with normal testicular function in the rat as determined by normal testosterone levels, tissue morphology and unchanged germ cell populations in the treated animals when compared to the controls.