HCV replicates in the hepatocytes, but it is not directly hepatotoxic. Lymphocytes recognize infected cells and initiate an immune response. Damage to the liver parenchyma is mediated by inflammatory cytokines, although the mechanism of disease progression is not clearly understood. Jain et al. and Pratico et al. have shown that oxidative stress may be a factor in progression to fibrosis and cirrhosis.8,9 It is believed that oxidative stress occurs via various mechanisms including the reduction of NAD to NADH that causes a redox change and inhibition of xanthine dehydrogenase activity resulting in a shift of purine oxidation to xanthine oxidase, thereby promoting the generation of oxygen-free radical species. A depletion in glutathione (GSH) has also been found in chronic liver disease which impairs defense against oxidative stress.10 Several other studies have attempted to evaluate for oxidative stress associated with HCV, but until recently accurate markers for evaluation of oxidative stress had not been determined. Studies attempting to treat chronic HCV with interferon and antioxidant combination have been inconclusive due inability to appropriately measure oxidative stress.11, 12