Int. J. Environ. Res. Public Health 2010, 7 1876 (p = 0.001). Mutations in two regions of the DRD2 gene (TaqI A and TaqI B), are associated with alcoholism and other drug use disorders [13]. Regarding this matter, a RFLP in the TaqI A1 allele is strongly associated with severe alcoholism. Another study demonstrated that the frequency of the A1 allele at DRD2 in descendants of alcoholic parents was significantly higher than in children of non alcoholics. It was also shown a significant association between the genotype at DRD4 and the children of alcoholic patients [16]. Although there is a wide range of candidate genes related to alcoholism, further studies are needed, not only to elucidate the genetic etiology of this entity, but to decipher therapeutic targets. 4. Pathophysiology Mechanisms implicated in alcohol-induced liver damage involve many biochemical reactions with different simultaneous pathways interacting with each other. These mechanisms involve enzymes, ROS, endotoxins, cytokines, immune system cells, and genetic predisposition to develop alcoholic liver disease [17,18]. Alcohol is metabolized by oxdative reactions to acetaldehyde and then converted to acetate through alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). ADH is quantitatively the most important enzyme capable of catalysing the conversion of ethanol to acetaldehyde. Figure 1. Main molecular mechanisms by which ethanol causes oxidative stress. NAD Nicotinamide adenine dinucleotide, NADH reduced form of NAD, AMP-K Adenosine monophosphate protein kinase, ROS Reactive oxygen species, ADH Alcohol dehydrogenase, ALDH Acetaldehyde dehydrogenase.