الفهرس 
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Abstract
Oxidative stress is a key in the development and progression of many HCV pathological conditions. HCV infection is characterized by increased markers of oxidative stress. Lipid peroxidation products are increased in serum, peripheral blood mononuclear cells (PBMC), and liver specimen from hepatitis C patients. Oxidants may kill target cells and overwhelm cellular antioxidant defenses of neighboring cells, leading to DNA damage Chronic over-production of reactive oxygen species leads to redox imbalance, favoring depletion of GSH, the major non-enzymatic antioxidant which has several physiological functions such as maintenance of protein-SH groups in a reduced state, detoxification from oxygen radicals, enzymatic degradation of endogenous peroxides, and formation of bioactive molecules. In consequence, reduced levels of plasma GSH are associated with development of liver fat diseases and cardiovascular diseases, and activation of viruses. There is a good correlation between type and severity of HCV and antioxidant level in the blood. So, patients with chronic HCV infection under the influence of oxidative stress showed lower levels of antioxidant enzymes. Also, there is a noticeable difference in oxidative stress in blood of HCV patients before and after treatment as Serum GSH decreases in patients who were not treated with interferon. In contrast, GSH concentration was higher in blood of patients responding satisfactorily to the treatment.