SUPPRESSION OF TESTOSTERONE AND ESTRADIOL-17-BETA-INDUCED DYSPLASIA IN THE DORSOLATERAL PROSTATE OF NOBLE RATS BY BROMOCRIPTINE

We, and others, have previously described the histological changes tha t occur in the prostate gland of intact Noble (NBL) rats following pro longed hormonal treatment. Dysplasia, a pre-neoplastic lesion, develop s specifically in the dorsolateral prostates (DLPs) of NBL rats treate d for 16 weeks with a combined regimen of testosterone (T) and estradi ol-17 beta (E-2) (T + E-2-treated rats), Concurrent with DLP dysplasia induction, the dual hormone regimen also elicits hyperprolactinemia, in addition to an elevation of nuclear type II estrogen binding sites (type II EBS), no alteration in estrogen receptors (ER), and marked ep ithelial cell proliferation in the dysplastic foci, The aim of this st udy was to investigate whether the dual hormone action is mediated via E-2-induced hyperprolactinemia, Bromocriptine (Br), at a dose of 4 mg /kg body wt per day, was used to suppress pituitary prolactin (PRL) re lease, Serum PRL levels were lowered from values of 341 +/- 50 ng/ml i n T + E-2-treated rats to 32 +/- 10 ng/ml in Br co-treated animals, Th e latter values were comparable to those in untreated control rats, In addition, Br co-treatment effectively inhibited the evolution of dysp lasia (six out of eight rats) and the often associated inflammation (f ive out of eight rats) in most animals, In contrast, Br co-treatment d id not suppress the T + E-2-induced type II EBS elevation nor alter ER levels in the DLPs of these rats, when compared with T + E-2-treated rats, These data extend the many previous studies that have detailed m arked influences of PRL on rat prostatic functions, However, the curre nt study is the first. to implicate PRL in prostatic dysplasia inducti on ill vivo.