Prostatic intraepithelial neoplasia (PIN) is widely considered as a premalignant lesion. A number of studies indicate that high-grade PIN (HGPIN) represents a premalignant lesion that could evolve into invasive adenocarcinoma (1,2). Molecular and immunohistochemical markers have been used to characterize the progression of human PIN. Some of these markers include: changes in the level of expression of genes that encode cell proliferation regulators, increase in cell proliferation, genetic instability, and the expression of antiapoptotic oncoproteins (1,2).

Several rat models for PCA have been developed (2-4). Morphological similarities between human PIN and dysplastic changes experimentally promoted in rodent prostates have been reported (2). These studies have provided substantial evidence implicating Cd as a prostate carcinogen (5), but the epidemiological data linking Cd and PCA are less convincing (5). Cd toxicity may induce changes in cellular homeostasis of essential metal ions, such as Cu, Zn, and Ca. Since there are similarities in the Zn and Cd transport characteristics, it has been suggested that these metals share a common transport mechanism (6). Also, it has been stated that Cd induces premalignant and/or invasive epithelial lesions in rat ventral prostate when administered in drinking water (2, 5).

The present study was undertaken to investigate whether treatment with Cd alone or in combination with Zn would induce changes in cell proliferation (PCNA expression), DNA apoptotic fragmentation, resistance to apoptosis (bcl-2 oncoprotein expression); and mutations on bcl-2 gene segments (PCR-SSCA).

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