ABSTRACT
This chapter reviews some of the chemistry of oxygen radicals, especially the critical role of iron, and to describe possible mechanisms by which alcohol can result in increased production of reactive oxygen intermediates. The elevated iron levels in the liver found in alcoholics are much less than those found in patients with idiopathic hemochromatosis. The chapter suggests a multitude of ways by which acute and chronic ethanol administration can induce oxidative stress to the liver. Sufficient levels of antioxidative enzymes and biochemicals are required to remove reactive oxygen intermediates or prevent their formation. Increased generation of reactive oxygen intermediates by microsomes after chronic ethanol treatment may contribute to the hepatotoxic actions of ethanol, as well as play a role in the perivenous toxicity associated with ethanol consumption. Synthesis of transferrin by hepatocytes may be decreased by ethanol, as has been found with several other plasma proteins synthesized and secreted by the liver.
