Quantitative and immunohistochemical evaluation of PCNA, androgen receptors, apoptosis, and Glutathione-S-Transferase P1 on preneoplastic changes induced by cadmium and zinc chloride in the rat ventral prostate.
BACKGROUND
This study was directed to evaluate the immunoexpression of markers for cell proliferation, apoptosis, nuclear androgen receptors, and Glutathione-S-Transferase P1 (GSTP1), in preneoplastic changes induced by cadmium chloride (Cd) and cadmium plus zinc chloride (Cd + Zn) in rat prostate.


METHODS
The following parameters were calculated in ventral prostate of normal rats and rats that received Cd or Cd + Zn in drinking water during 24 months: numerical densities of columnar, basal, and GSTP1 immunoreactive epithelial cells; percentages of cells immunoreactive to: PCNA, (LI(PCNA)), androgen receptors (LI(AR)), and of apoptotic cells.


RESULTS
The LI(PCNA) was significantly increased in the animals exposed to Cd + Zn, whereas the numerical densities of both columnar (N(V) columnar cells), and GSTP1 immunoreactive (N(V) GSTP1+) cells were significantly increased in the animals treated with metals in comparison with the controls. No significant differences between the two sources of dysplasias (Cd and Cd + Zn) respecting to LI(PCNA), N(V) columnar cells, and N(V) GSTP1+ were observed. The two types of dysplasias considered together showed a significant increase for the N(V) basal, N(V) columnar, and N(V) GSTP1+ cells in comparison with normal acini of treated and controls. The percentage of apoptotic nuclei did not show significant differences among the three groups studied.


CONCLUSIONS
(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.
Arriazu
Riánsares
R
Department of Physiology, Morphology, and Nutritional Sciences, San Pablo-CEU University, Madrid, Spain.
Pozuelo
José M
JM
Martín
Rocío
R
Rodríguez
Rosario
R
Santamaría
Luis
L
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015415:Biomarkers; D002104:Cadmium / Q000633:toxicity; D002455:Cell Division / Q000187:drug effects; D002712:Chlorides / Q000633:toxicity; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase / Q000378:metabolism*; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D018384:Oxidative Stress; D011230:Precancerous Conditions / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism*; D019048:Prostatic Intraepithelial Neoplasia / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011944:Receptors, Androgen / Q000378:metabolism*; D017967:Zinc Compounds / Q000633:toxicity
D015415:Biomarkers; D002712:Chlorides; D007527:Isoenzymes; D018809:Proliferating Cell Nuclear Antigen; D011944:Receptors, Androgen; D017967:Zinc Compounds; D002104:Cadmium; C016837:zinc chloride; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; C496558:Gstp1 protein, rat