ABSTRACT
The direct action of ethanol on reactive oxygen intermediates (ROI) production has been clearly implicated in ethanol toxicity; however, several studies have demonstrated a role for acetaldehyde in the oxidative damage. All tissues in the body are affected by exposure to ethanol, and variations in the toxic effects may be a reflection of the ROI/reactive nitrogen intermediates generating mechanisms available in that tissue as well as the level of antioxidant protection. Diminished energy production and the formation of free radicals following hypoxia are believed to underlie cellular damage and the ensuing teratogenic effects. The effect is varied, however, and depends on the duration of exposure, the concentration of alcohol, and the type of agent used to induce ROI production. Although alcohol-induced oxidant stress and the consequent tissue injury have been described, little is known about the mechanisms by which ethanol induces tissue damage.
