Abstract
BACKGROUND: Oxidative stress could play a role in pathogenesis of hepatitis C virus (HCV) infection. The aim of our study is to determine oxidant/antioxidant status of patients with chronic hepatitis C (CHC), and the effect of pegylated interferon alfa-2b plus ribavirin combination therapy on oxidative stress. METHODS: Nineteen patients with chronic HCV infection and 28 healthy controls were included in the study. In control and patient groups, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, erythrocyte malondialdehyde (MDA) levels, erythrocyte CuZn-superoxide dismutase (SOD), erythrocyte glutathione peroxidase (GSH-Px) activities were measured. After pegylated interferon alfa-2b and ribavirin combination therapy for 48 weeks, these parameters were measured again in the patient group. RESULTS: Serum MDA levels increased significantly in CHC patients (n:19), before the treatment when compared with healthy subjects (n:28) 9.28 +/- 1.61, 4.20 +/- 1.47 nmol/ml, p < 0.001 respectively. MDA concentration decreased significantly (p < 0.001) after the treatment as well as ALT, AST activity, in erythrocytes of these patients. Average antioxidant enzymes (superoxide dismutase and glutathione peroxidase) were significantly lower in erythrocytes of patients with CHC before treatment compared with the control group (both, p < 0.001). Chronic Hepatitis C patients after pegylated interferon alfa-2b and ribavirin therapy showed values of SOD, GSH-Px were significantly higher than pretreatment levels (both, p < 0.001). CONCLUSION: Our results show that patients with chronic HCV infection are under the influence of oxidative stress associated with lower levels of antioxidant enzymes. These impairments return to level of healthy controls after pegylated interferon alfa-2b plus ribavirin combination therapy of CHC patients. Although interferon and ribavirin are not antioxidants, their antiviral capacity might reduce viral load, and inflammation, and perhaps through this mechanism might reduce virus-induced oxidative stress.