It is known that during oxidative stress conditions the levels of oxidants are higher than the levels of antioxidants [17,18]. Besides mitochondrial oxidative phosphorylation, the cellular activation of NADPH/xanthine oxidase (NOX/XOX) or nitric oxide synthase and copper/iron-catalyzed Fenton-Weiss-Haber (FWH) reaction of H2O2 [19] also produce oxidants. Alcohol-induced ROS production is believed to be specific to EtOH metabolism by cytochrome P450-2E1 (CYP2E1), which produces H2O2 in addition to acetaldehyde (Ach), while alcohol dehydrogenase (ADH) mediated produces only Ach. Interaction of H2O2 with copper/iron produces ROS during EtOH oxidation by alcohol-inducible liver microsomal cytochromes P-450 enzymes [19,20]. Cederbaum and colleagues showed that metabolism of EtOH by CYP2E1 causes oxidative liver damage by increased ROS levels [21,22] and by reduction of glutathione and superoxide dismutase activity [23,24].
