No abstract

(1) The zinc has little influence in the development of the dysplastic changes of the rat prostate mediated by cadmium. (2) The decrease of apoptosis has little influence in the development of dysplasia. (3) GSTP1 could play a role in the response to the oxidative stress in the dysplastic changes caused by cadmium.

No abstract

This work was directed to evaluate immunoexpression of markers for apoptosis, resistance to apoptosis, and cell proliferation, as well as estimates of nuclear size in ventral prostate of rats treated with cadmium chloride and cadmium+zinc chloride because a possible protective effect of zinc has been postulated. The following variables were studied: volume fraction (VF) of Bcl-2 immunostaining, percentage of cells immunoreactive to proliferating cell nuclear antigen (LIPCNA) and p53 (LIp53), numerical density of caspase-3 immunoreactive cells (NV caspase-3), and estimates of volume-weighted mean nuclear volume (upsilonV). The LIPCNA and VF of Bcl-2 were significantly increased in the treated animals. The dysplasias (independent of their origin) showed a significant increase of the LIp53, NV caspase-3, and upsilonV in comparison with normal acini from treated and control animals. It can be concluded that cell proliferation is enhanced in long-term cadmium-exposed rats, and exposure to zinc combined with cadmium had no effect on any of the variables studied when comparing with normal acini. The increase of nuclear upsilonV could indicate a more aggressive behavior for pretumoral lesions.

PNEC differ in rats when compared to humans: they are weakly immunopositive to cgA, do not express PGP 9.5, only show immunoreactivity to SER, and do not appear in acini. The changes in the amount of rat PNEC during the post-natal development suggest an androgenic influx. PNEC might regulate the contractility of periurethral ducts.