BACKGROUND: Ethanol may increase the production of reactive oxygen species(ROS) in the liver, which results in the development of alcoholic liver disease (ALD). Cytokine-activatedblood leukocytes may also participate in this process. The aim of our study was to evaluate the oxidativestress level in the blood of patients with alcoholic liver cirrhosis.MATERIAL/METHODS: Blood neutrophilsfrom 16 patients with compensated alcoholic liver cirrhosis and 28 patients with decompensated were evaluatedfor their ability to produce superoxide anion and hydrogen peroxide spontaneously and after PMA induction,in comparison to controls (16 healthy persons). Serum catalase (CAT), superoxide dismutase (SOD) andglutathione peroxidase (GPx) activity were also measured in both groups of patients and in the controls.RESULTS:The neutrophils from patients with compensated liver cirrhosis spontaneously produced a normal levelof O2*- and a high level of H2O2, but exhibited a defect in PMA-induced O2*- production. The neutrophilsfrom patients with decompensated liver cirrhosis spontaneously produced more O2*- and H2O2 than the controls,but the PMA response was weak. There were no changes in the expression of GPx, but enhanced SOD activitywas observed in the serum of patients with decompensated alcoholic liver cirrhosis. Increased CAT activitywas detected only in serum from patients with compensated liver cirrhosis.CONCLUSIONS: These data pointto oxidative stress in the blood of patients with decompensated alcoholic cirrhosis, since increasedresting production of ROS in neutrophils was not accompanied by increased GPx and CAT activity in serum.

Keywords: Liver Cirrhosis, Alcoholic