Oxidative stress has been increasingly implicated in the pathogenesis and progression of liver cirrhosis.Chronic ethanol consumption induces an oxidative stress resulting in increased ferritin levels and thereby iron over load. The study was aimed at evaluating the relation between alcohol consumption and erythrocyte superoxide dismutase (SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA) activities in liver cirrhosis patients. The study included two groups based on alcohol consumption; subjects taking low alcohol content (Less than 150 g/day.), those consuming high alcohol content (More than 150 g/day), diagnosed as suffering from liver cirrhosis and control group who do not take alcohol and are not suffering from liver cirrhosis. All cirrhotic patients on high alcohol intake in the study group had lower serum SOD (P < 0.0001), GPx (0.0001) and significantly higher MDA levels (P<0.001) than those with subjects taking low alcohol and control group. These results suggest that the decrease in erythrocyte SOD, GPx and increase in MDA levels are related to the alcohol consumption and that may be associated with pathogenesis and progression of liver disease.

Oxidative stress has been increasingly implicated in different stages of liver cirrhosis and has been found responsible for DNA damage. Alcohol consumption and oxidative stress have been linked with DNA damage and progression of disease, leading to the hypothesis that chronic alcoholism causes DNA damage. The study was aimed at evaluating the relation between alcohol consumption and relative oxidative damage in different stages of liver cirrhosis. The study included two groups based on severity of cirrhosis of liver; categorized as compensated and decompensated liver cirrhotic patients based on child Pugh criteria. All decompensated cirrhotic patients in the study group had significantly higher MDA levels (P < 0.001) associated with DNA Damage (P > 0.01) than those with compensated cirrhotic patients and control group who were not suffering from liver cirrhosis. These results highlighted a significant higher degree of DNA damage in decompensated cirrhotic patients associated with oxidative stress as shown from greater average DNA migration in decompensated cirrhotic patients than in the compensated cirrhotic patients with low level of oxidative stress. Thus these results suggest that increase in MDA levels may be associated with pathogenesis and progression of liver cirrhosis.

Alcohol is detoxified in the liver by the enzymes alcohol dehydrogenase and aldehyde dehydrogenase. The available literature suggests that activity of aldehyde dehydrogenase is less than alcohol dehydrogenase among Asians; hence it leads to accumulation of acetaldehyde during excess intake of alcohol. Accumulated acetaldehyde due to its electrophilic nature forms adducts with proteins and DNA. The acetaldehyde-DNA adduct (N-2-Ethyl deoxyguanosine (NDG)) induces mutations in DNA and leads to DNA damage. Prevention of excessive accumulation of acetaldehyde can be useful in decreasing the genotoxicity.