Abstract
Damage of hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected hepatocytes is mediated by both a direct cytopathic effect of the viruses and by immunologic response of T-cells, However, other mechanisms such as oxidative stress, may also be involved in cellular damage. We conducted a study to investigate the status of superoxide dismutase activity (SOD) and the total antioxidant status (TAS) in a consecutive cohort of patients infected with HBV and HCV infections, including HBV patients in the chronic inactive state of the disease. The latter were included in an attempt to determine whether antioxidant status is affected even in cases where an obvious viral activity is absent. TAS and SOD were measured in 55 patients (43 HBV, 12 HCV) and 25 healthy controls. 17 out of 43 patients had chronic inactive HBV state, 15 had chronic hepatitis Band 11 had HBV-related cirrhosis. In the HCV group, 6 patients had chronic hepatitis C and 6 HCV-related cirrhosis. Erythrocyte SOD activity was determined in haemolysate from red blood cells using a kinetic spectrophotometer method. TAS was measured by a colorimetric assay. The mean TAS and SOD values in the total number of patients (1.20±0.12 mmol/L and 1040±255 Ulg Hb, respectively) were significantly lower (p<0.001) compared to healthy controls (1.57±0.13 mmol/L and 1491±420 D/g Hb), Comparisons between groups showed significantly lower (p<0.001) TAS and SOD values in each subgroup of patients compared to healthy controls. A significant positive correlation was found between TAS and SOD in the total number ofpatients (n= 55, p<0.01), in the chronic hepatitis group (n=21, p=0.01) and in the total group of HBV patients (n=43, p<0.01). We demonstrated a significant reduced antioxidant capacity in patients with chronic HBV and HCV as indicated by low TAS and SOD. These findings were independent of the virological, biochemical and clinical status of the patients, including those with chronic inactive HBV state. This could suggest that the tissue-related consequences of oxidative stress might start from the inactive stage of liver viral diseases. However, our observations should be viewed with caution and need to be tested in a larger numbers of patients in order to determine prospectively whether these findings have pathophysiological and/or clinical significance.