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From the * Department of Anatomy, Cell Biology,
Physiology, and Biophysics, Institute of Biology, State University of Campinas
(UNICAMP), Campinas SP, Brazil; and the
Department of Animal Reproduction, College of
Veterinary Medicine and Animal Sciences, University of São Paulo,
São Paulo SP, Brazil.
| Correspondence to: Hernandes F Carvalho, Department of Anatomy, Cell Biology, Physiology, and Biophysics–UNICAMP, CP6109, 13083-863 Campinas SP, Brazil (e-mail: hern{at}unicamp.br). |
Prostate growth and physiology are regulated by steroid hormones and
modulated by multiple endocrine factors. We investigated the action of insulin
on the tissue organization and kinetics of epithelial cells in the rat ventral
prostate (VP) in response to castration up to 120 hours after surgery by using
an acute protocol of alloxan-induced diabetes. Diabetes caused a reduction in
volume density (Vv%) and volume of the epithelium. The effects of
castration on the epithelium were accelerated in the diabetic animals, as
determined by changes in Vv% and volume. The smooth muscle cells
became atrophic and apparently relaxed in response to castration, in contrast
to the spinous aspect observed in nondiabetic castrated rats. Counting of
apoptotic nuclei in the epithelium showed the classical apoptosis peak at 72
hours in nondiabetic rats and an advance of the apoptosis peak to 48 hours
after castration in diabetic rats. Insulin restored the time of the peak to 72
hours. These results were confirmed after immunostaining for cleaved caspase-3
and suggest a survival and antiapoptotic effect on VP epithelial cells in both
the presence and absence of androgen stimulation. This idea is supported by
the observation that insulin also reduced the overall rate of apoptosis at all
experimental points analyzed before and after castration.
Key words: Apoptosis, tissue remodeling
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