Abstract
A line of rats with defects in reproduction (BIL/1 or BY1 strains) has been studied to determine whether the defects in spermatogenesis were due to an insufficiency of either gonadotropins or steroids. In the aspermatic male, no deficiencies in circulating LH, FSH, or testosterone were observed. The regulatory mechanisms controlling the serum concentrations of these hormones were intact as shown by the ability of the pituitary gland to respond appropriately to either a decrease or an increase in circulating testosterone. An androgen-dependent tissue (prostate) was capable of normal metabolism and localization of steroids, and no abnormalities were observed in prostate, seminal vesicles, or preputial gland when examined histologically. Various cellular components of the testis were capable of binding exogenous gonadotropins, and exogenous LH administration resulted in a normal response as measured by increased testosterone secretion. The normal intratesticular temperature suggested that aspermatogenesis was not due to an abnormally increased testicular temperature. These experiments exclude certain endocrine parameters as the causative agent in this genetically controlled defect in spermatogenesis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
