INTRODUCCIÓN La hepatopatía relacionada con el consumo de alcohol puede clasificarse en tres categorías distintas: hígado gra-so, hepatitis alcohólica y cirrosis. El hígado graso, que se produce tras la ingesta prolongada de alcohol, es normalmente reversible con la abstinencia y no predispone a padecer ninguna forma crónica de enfermedad hepática, siempre que se mantenga la abstinencia o la moderación (1). La hepatitis alcohólica es una forma aguda de lesión hepática inducida por el alcohol

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... o espectro de gravedad va del desequilibrio asintomático de la bioquímica hepática a la insuficiencia hepática y la muerte. La aparición de una hepatitis alcohólica generalmente implica el consumo de una gran cantidad de alcohol durante un periodo de tiempo prolongado, a veces de años (2). La ci- ABSTRACT Acute and chronic alcohol consumption increases the production of reactive oxygen species (ROS), and enhances lipid peroxidation of lipids, proteins, and DNA. The mechanism by which alcohol causes cell injury is still not clear but a major role for ROS and lipid peroxidation-end products is considered. Many pathways have been suggested to play a role on how ethanol induces a state of "oxidative stress", including redox-state changes, acetaldehyde production, damage to mitochondria, membrane injury, apoptosis, ethanol-induced hypoxia, effects on the immune system and altered cytokine production, increased endotoxin levels and activation of Kupffer cells, mobilization of iron, modulation of the antioxidant defense, particularly mitochondrial glutathione (GSH), one electron oxidation of ethanol to 1-hydroxy-ethyl radical, and induction of CYP2E1. These pathways are not exclusive of one another and it is likely that several, indeed many, systems contribute to the ability of ethanol to induce a state of oxidative stress.