الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
The pathogenesis mechanism of viral hepatitis (C and B) is closely related to hepatocyte necrosis as well as apoptosis. Apoptosis is a physiologic form of cell death which implicated in the regulation of the number of cells in various tissues. The hepatic tissue homeostasis depends on maintaining the balance between cell proliferation and apoptosis and disruption of this balance may contribute to hepatic carcinogenesis.
Apoptosis of liver cells may play a significant role in the pathogenesis of viral hepatitis (C,B). The hepatitis C virus (HCV) core protein exhibits both proapoptotic and antiapoptotic actions also upon hepatitis B virus infection, HBx protein sensitizes liver cells to apoptosis which contribute to the development of chronic hepatitis and the subsequent generation of hepatocellular carcinoma. Further analysis suggested that cell death occurred through the activation of p53 proapoptotic and antiapoptotic Bcl-2 protein pathways.
The harmful action of oxidative free radicals was minimized by a defensive antioxidant enzyme mechanisms including (superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione).The presence of excess oxygen radicals or inhibitions of antioxidant enzymes may participate in the regulation of programmed cell death. Malondialdehyde (MDA) is lipid peroxide free radical, whose content usually reflects lipid peroxidation and the extent of liver cell injury in vivo. Also, NO free radical was found to act as protecter against liver injury by scavenging lipid radicals and inhibiting the lipid peroxidation chain or may potentiate liver cytotoxicity by reaction with superoxide anion to form peroxinitrite which promotes nitration of tyrosine to form nitro tyrosine whereas its interahepatic accumulation is associated with the severity of liver necrosis and cell death