Introduction Alcoholic liver disease (ALD) is due to the abusive consumption of alcohol, the major cause of morbidity and mortality associated with liver disease (Gramenzi et al., 2006) and one of the greatest health problems in the world (Singha et al., 2007). Over the last few years, several studies have clarified important immunological and metabolic consequences of excessive alcohol consumption that may contribute to liver pathogenesis (Stewart et al., 2001). Increased oxidative stress and the modulation of the redox state of the cell are among the most extensively studied consequences of alcohol consumption (Gyamfi et al., 2008; Ramírez-Farías et al., 2008). After ingestion, alcohol is metabolized in the liver by two pathways. The first involves its transformation to acetaldehyde by the action of the enzyme alcohol dehydrogenase (ADH) located in the cytosol and is followed by transformation to acetate predominantly due to the action of the Scand.