Antioxidant nutrients and alcohol.

Alcohol is a constituent of the diet that is generally taken in on a voluntary basis. The amount and type of alcohol consumed along with the frequency of alcohol consumption can vary tremendously and can have divergent effects on an organism. Animal models have been developed to investigate the mechanisms by which both acute alcohol administration and chronic alcohol consumption affect the various organ systems of the body. The deleterious effects of alcohol, at least partly involve alcohol induced oxidative injury that has been documented by measurement of oxidant radicals, alterations in oxidant/antioxidant balance and oxidant induced changes in cellular proteins and lipids. In addition, evidence for alcohol-induced oxidant injury comes from studies in which pretreatment with antioxidants such as vitamin E, vitamin C, and agents that enhance antioxidant capacity attenuate alcohol induced effects. The susceptibility of tissues to alcohol-induced injury is related to their function and the method by which they are exposed to alcohol. For example, the stomach and liver are exposed to the highest concentrations upon ingestion and absorption of alcohol. The liver is also the major organ for metabolism, and with chronic alcohol use, P450 2E1 is induced. This enzyme activity however, adds additional oxidative stress to the liver. Although antioxidants can attenuate alcohol-induced injury, there is no one antioxidant that protects all organs during all modes of exposure. In addition, more studies are needed to determine if administration of antioxidants after alcohol exposure can reverse alcohol induce tissue damage. This review will summarize results from experiments in which alcohol has been delivered for a short time (acute) or prolonged period (chronic); in vivo or in vitro; at physiologic doses or at supraphysiologic doses. The effects of alcohol on various tissues will be presented and finally, the contribution of oxidant injury to alcohol induced tissue damage will be discussed.