CONICET | Buscador de Institutos y Recursos Humanos

Previous studies showed that cytosolic and microsomal fractions from rat ventral prostate are able to oxidize ethanol to acetaldehyde and 1-hydroxyethyl radicals. Sprague Dawley male rats were fed with a Lieber & De Carli diet containing ethanol for 28 days and compared against adequately pair fed controls. Microsomal fractions were found to exhibit CYP2E1-mediated hydroxylase activity significantly lower than in liver and that was induced by repetitive ethanol drinking. Ethanol drinking led to increased susceptibility of lipids to oxidation as detected by t-butylhydroperoxide-promoted chemiluminiscence emission and increased levels of lipid hydroperoxides. However, no depletion in the GSH content was observed and a highly significant finding was the increased activity of glutathione peroxidase, glutathione reductase and glutathione transferase in the prostate of treated animals. Ultrastructural alterations in the epithelial cells were observed, consisting of a condensation of chromatin around the perinuclear membrane, moderate dilatation of their endoplasmic reticulum and an increased number of epithelial cells undergoing apoptosis. Prostatic ADH activity of our stock rats was 4.84 times smaller than that in liver and ALDH activity in their microsomal, cytosolic and mitochondrial fractions was significantly less intense than in liver. A single dose of ethanol led to significant acetaldehyde accumulation in the prostate. Results suggest that acetaldehyde accumulation in prostate tissue might result from both acetaldehyde produced in situ but also because of its low aldehyde dehydrogenase activity and its poor ability to metabolize acetaldehyde arriving via blood. Acetaldehyde, 1-hydroxyethyl and the oxidative stress produced may lead to epithelial cell injury.