Direct effects of estrogens on the endocrine function of the mammalian testis.
This article reviews literature relevant to the view that estradiol (E2) synthesized in the testis acts locally to modify testosterone secretion. Despite a lack of convincing evidence from in vitro experiments, in vivo experiments with intact and hypophysectomized animals have demonstrated that estrogens can inhibit testosterone secretion by acting directly on the testis. Reduced testosterone production in estrogen-treated animals probably results from reduced 17 alpha-hydroxylase and (or) C17-C20 lyase activity. Estrogen-inhibited steroidogenesis may result from estrogen binding to high affinity--low capacity estrogen receptors. Besides being an estrogen target tissue, the testis produces E2; the cellular site of testicular E2 synthesis remains controversial. Recent studies indicate that E2 is synthesized primarily in the Sertoli cells of neonatal rats and in the Leydig cells of older rats. Follicle-stimulating hormone and human chorionic gonadotropin (hCG) increase testicular aromatase activity and E2 concentrations in neonatal and older rats, respectively. An increase in testicular E2 concentrations, following hCG administration, may be one mechanism by which testosterone synthesis becomes desensitized to subsequent hCG stimulation. However, whether gonadotropin-stimulated testicular E2 synthesis is part of a physiologically relevant "short" feedback loop that participates in the regulation of testosterone synthesis remains to be determined.
D000728:Androgens / Q000378:metabolism; D000818:Animals; D004967:Estrogens / Q000494:pharmacology*; D005246:Feedback; D007016:Hypophysectomy; D007986:Luteinizing Hormone / Q000494:pharmacology; D008297:Male; D051381:Rats; D011960:Receptors, Estrogen / Q000378:metabolism; D013737:Testis / Q000187:drug effects* / Q000378:metabolism
D000728:Androgens; D004967:Estrogens; D011960:Receptors, Estrogen; D007986:Luteinizing Hormone