Abstract
This chapter discusses the general aspects of alcohol metabolism. Catalase— located in the peroxisomes was known to break down ethanol, but it is now realized that this is a minor pathway. The main pathway proceeds via cytosolic alcohol dehydrogenase (ADH) that has multiple isoenzymes, the genetic polymorphism of which is now being unraveled in terms of its possible clinical implications. The latest ADH isozyme to be fully characterized is sigma ADH that is prevalent in the upper gastrointestinal (GI) tract and exhibits ethnic variability. A third pathway of ethanol metabolism was discovered— the Microsomal Ethanol Oxidizing System (MEOS) which, contrary to the two other pathways, is highly inducible by chronic alcohol consumption, with a 4–10-fold increase of cytochrome P4502E1 (CYP2E1). It is associated with proliferation of the endoplasmic reticulum, both in experimental animals and in humans. This induction contributes to the metabolic tolerance against ethanol that develops in alcoholic and spills over to other drugs, which are microsomal substrates. Administration of ethanol with nondeficient diets resulted in accelerated blood clearance not only of ethanol but also drugs that persisted for days to weeks after the cessation of alcohol, depending on the drug.
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