Carcinogenesis, Vol 18, 1505-1510, Copyright © 1997 by Oxford University Press
KE Lane, I Leav, J Ziar, RS Bridges, WM Rand and SM Ho
We, and others, have previously described the histological changes that
occur in the prostate gland of intact Noble (NBL) rats following prolonged
hormonal treatment. Dysplasia, a pre-neoplastic lesion, develops
specifically in the dorsolateral prostates (DLPs) of NBL rats treated for
16 weeks with a combined regimen of testosterone (T) and estradiol-17beta
(E2) (T + E2-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 epithelial cell
proliferation in the dysplastic foci. The aim of this study was to
investigate whether the dual hormone action is mediated via E2-induced
hyperprolactinemia. Bromocriptine (Br), at a dose of 4 mg/kg body wt per
day, was used to suppress pituitary prolactin (PRL) release. Serum PRL
levels were lowered from values of 341 +/- 50 ng/ml in T + E2-treated rats
to 32 +/- 10 ng/ml in Br co-treated animals. The latter values were
comparable to those in untreated control rats. In addition, Br co-treatment
effectively inhibited the evolution of dysplasia (six out of eight rats)
and the often associated inflammation (five out of eight rats) in most
animals. In contrast, Br co-treatment did not suppress the T + E2- induced
type II EBS elevation nor alter ER levels in the DLPs of these rats, when
compared with T + E2-treated rats. These data extend the many previous
studies that have detailed marked influences of PRL on rat prostatic
functions. However, the current study is the first to implicate PRL in
prostatic dysplasia induction in vivo.
ARTICLES
Suppression of testosterone and estradiol-17beta-induced dysplasia in the dorsolateral prostate of Noble rats by bromocriptine
Department of Biology, Tufts University, Medford, MA 02155, USA.
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