Hyperprolactinemia inhibits development of Leydig cell tumors in aging Fischer rats.
In inbred CDF (Fischer 344) male rats autopsied at the age of 18-24 months, testicular tumors were present in 24 of 36 control animals but in none of 28 males rendered hyperprolactinemic by transplantation of anterior pituitaries from adult females under the renal capsules. In another experiment, microscopically detectable Leydig cell adenomas were present in each of 11 control animals at the age of 14.5 months but in none of 11 males in which hyperprolactinemia was induced by treatment with diethylstilbestrol. Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles. Incubated tumor tissue produced large quantities of progesterone and responded to hCG in vitro by an increase in progesterone but not testosterone secretion. Daily sperm production and epididymal sperm reserves were significantly reduced already during early stages of Leydig cell tumor development. We propose that hyperprolactin prevents development of Leydig cell tumors by suppression of plasma LH levels and suggest that age-related reductions in gametogenic and steroidogenic functions of the testes in Fischer rats are due to development of Leydig cell tumors rather than to aging per se.
D000367:Age Factors; D000735:Androstenedione / Q000097:blood; D000818:Animals; D004054:Diethylstilbestrol / Q000494:pharmacology; D006966:Hyperprolactinemia / Q000473:pathology*; D007984:Leydig Cell Tumor / Q000473:pathology*; D008297:Male; D011374:Progesterone / Q000097:blood; D051381:Rats; D011916:Rats, Inbred F344; D013076:Sperm Count; D013091:Spermatogenesis / Q000187:drug effects; D013736:Testicular Neoplasms / Q000473:pathology*; D013737:Testis / Q000473:pathology; D013739:Testosterone / Q000097:blood
D013739:Testosterone; D000735:Androstenedione; D011374:Progesterone; D004054:Diethylstilbestrol