الفهرس 
Introduction and aim of workOnly 14 pages are availabe for public view
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Abstract
Background: Hepatic iron concentration (HIC) has been shown to be only mildly to moderately elevate in hepatitis C virus (HCV) infection. The pathogenic role of hepatic iron via the generation of oxidative stress is well established. Iron mediates this process by catalyzing the production of reactive oxygen species (ROS) through the Fenton reaction. Moreover, ROS are known to disrupt protein structure and may cause DNA damage, which may eventually lead to hepatocellular carcinoma (HCC).Therefore, this study was performed to describe the current understanding of the relationship between hepatic iron, serum iron indices and role of hepatic iron in the generation of oxidative stress in relation to progression of liver disease in chronic hepatitis C. Methods: Fifty patients were divided into three groups according to Metavir staging (Scoring system for the assessment of fibrosis): Twenty patients with fibrosis (F≤3), Fifteen patients with cirrhosis (F=4), and Fifteen patients with hepatocellular carcinoma. They are compared with group of Twenty individuals free from any disease were taken as controls. Therefore, the free radicals utilizing enzymes including superoxide dismutase (SOD), in addition to malonaldhyde (MDH), and glutathione content (GSH) as well as hepatic iron, serum iron and transferring saturation were investigated. Results: A marked increase in hepatic iron concentration, serum ferritin, serum iron and transferrin saturation were observed in patients with liver fibrosis (F≤3), liver cirrhosis (F=4) and in patients with HCC. On the other hand, a marked reduction of superoxide dismutase (SOD) activity and reduced glutathion (GSH) level were observed in blood of patients of study and this associated with the high level of malondialdehyde (MDA).These results indicate that the loss of SOD activities may be a causative factor of more cellular damage of these patients. Conclusions: Iron accumulation in HCV-related chronic hepatitis is clinically relevant in increasing oxidative stress, which is correlated with hepatic fibrosis, inflammation and carcinogenesis.