Viral hepatitis, primarily caused by hepatitis B virus (HBV) and hepatitis C virus (HCV), is a leading cause of chronic liver disease worldwide. Accumulating evidence suggests that oxidative stress (OS) plays a pivotal role in the pathogenesis and progression of viral hepatitis. OS occurs due to a disproportion between reactive oxygen species (ROS) generation and antioxidant protection, resulting in damage to cells and tissues. In viral hepatitis, viral proteins and immune-mediated inflammatory responses contribute to excessive ROS generation, resulting in oxidative damage to hepatocytes. This damage manifests as lipid peroxidation, DNA damage, and protein oxidation, which in turn promote hepatic inflammation, fibrosis, and hepatocellular carcinoma. Furthermore, OS has been implicated in the resistance to antiviral therapy observed in some patients. This review highlights the molecular mechanisms underlying OS in viral hepatitis, its contribution to liver disease progression, and its impact on treatment outcomes. Understanding these mechanisms may open new avenues for therapeutic strategies targeting OS, thereby improving the management of viral hepatitis and associated liver diseases.
Key words: Oxidative Stress; Viral Hepatitis; Hepatitis C
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