Lipid Peroxidation in Hepatic Fibrosis

Damage of any etiology, such as infection with hepatitis C virus (HCV) or hepatitis B virus (HBV), heavy alcohol intake, and iron overload, to hepatocytes can produce oxygen-derived free radicals and other ROS derived from lipid peroxidative processes. Persistent production of ROS constitutes a general feature of a sustained inflammatory response and liver injury, once antioxidant mechanisms have been depleted. The major source of ROS production in hepatocytes is NADH and NADPH oxidases localized in mitochondria (Figure 1). NADH and NADPH oxidases leak ROS as part of its operation. Kupffer cells (hepatic resident macrophages), infiltrating inflammatory cells such as macrophages and neutrophils, and HSCs also produce ROS in the injured liver.