Antioxidant status and alcohol-related diseases.

Chronic ethanol consumption is associated with increased incidence of a variety of illnesses, including cancer. Studies have shown that ethanol consumption may result in increased oxidative stress with formation of lipid peroxides and free radicals. The susceptibility of a given tissue to peroxidation is, however, a function of the overall balance between prooxidants and antioxidant defence systems. The latter involve both intracellular and extracellular protective factors were nutrients play an important role. Impaired nutritional status of different vitamins and trace elements have been reported in alcoholics. Reduced levels of vitamin E have been found in serum of alcoholics with and without liver disease and in liver biopsies from alcoholics with cirrhosis. These findings may be due to the increased oxidative stress as reported in experimental animals, and may be of importance since vitamin E is the major, if not the only, lipid-soluble free radical scavenger in some tissues. Reduced antioxidant capacity has been found in several tissues and may promote the generation of free radicals and lipid peroxides which may damage cells directly, induce inflammation and accelerate collagen synthesis. These events may progress to tissue damage and disease. The importance of radicals in cancer initiation and promotion is presently of great interest. The role of lipid peroxides and free radicals in alcohol-related disease and cancer remains unresolved. Further research is required to establish the role of these reactive species in the pathogenesis of alcohol-related disease, and to evaluate the role of nutrition in favour of the antioxidant defence mechanisms.