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Biology of Reproduction, Vol 23, 564-569, Copyright © 1980 by Society for the Study of Reproduction
1 Department of Pathology and Department of Physiology,
University of Pittsburgh School of Medicine,
Pittsburgh, Pennsylvania 15261 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.
Accepted on July 14, 1980
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