Gastrointestinal Tract Including Carcinogenesis

The role ofROS in alcohol-associated gastric mucosal injury is underlined by the fact that oral administration of absolute alcohol to rats reduces glutathione and increases lipid peroxidation in the gastric mucosa [105], Antioxidants, superoxide dismutase and hydroxyl radical scavengers prevent gastric lesions caused by alcohol, whereas inhibition of superoxide dismutase results in a deterioration [105], It is interesting to note that the pretreatment of rats with allopurinol, a xanthine oxidase inhibitor, protects against haemorrhagic lesions due to alcohol which points to the involvement ofROS produced by xanthine oxidase in the gastric mucosa [106,107], However, controversial results have also been published by using a stomach perfusion model with 30% alcohol [108], In any event, cellular glutathione levels are believed to be indicators of oxidative tissue injury and it has been shown in experimental animals as well as in humans that alcohol decreases gastric mucosal glutathione concentrations.

Chronic alcohol consumption is associated with an increased risk of cancer in the upper alimentary tract and the colorectum [109], It might be possible that the production ofROS is involved in alcohol-associated carcinogenesis since chronic alcohol consumption leads to an induction of cytochrome P450 in the oral mucosa in the esophagus and in the colon of rodents [110,111], Such an induction can also be demonstrated in the human oral mucosa [112]. In addition, the presence of xanthine oxidase has been located in the epithelial cells of the mouse and of the esophagus [113]. In an experiment by Eskelsson and co-workers, it has been shown that the number of esophageal tumors induced by nitrosamines and stimulated by chronic alcohol administration can be significantly reduced by the concomitant application of vitamin E [114]. Furthermore, this reduction is associated with a reduction in lipid peroxidation products in the esophagus. This is indirect evidence for the involvement ofROS in alcohol associated esophageal carcinogenesis. Mucosal hyperproliferation due to alcohol is a premalignant condition and we have recently observed that vitamin E supplementation to rats leads to a normalization of colorectal cell regeneration [115]. Thus, there is some indirect evidence that vitamin E supplementation, at least in rodents, may be helpful in alcohol-associated cancer prevention.

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