Oxidative stress and antioxidants in hepatic pathogenesis

Figure 1 Increased reactive oxygen species in hepatitis B virus X protein transfected HepG2 stable cell line and hepatitis B virus X protein transgenic mouse hepatocytes. Reactive oxygen species (ROS) was detected by FACS caliber using dichlorofluorescein diacetate (DCFA-DA). A: HepG2 cell line stably transfected with hepatitis B virus X protein (HBx) showed a higher level of ROS compared to control cells; B: ROS production was checked after 4 wk of male HBx and control mouse hepatocyte growth. HBx mice hepatocytes generate more ROS than control mice.

Figure 2 Chronic ethanol consumption caused liver damage in hepatitis B virus X protein transgenic mice. Ethanol fed hepatitis B virus X protein (HBx) tg mouse liver (B) showed severe liver damage, hepatocyte enlargement and fatty changes compared with water fed HBx (A). Original magnifications 100 ×.

Figure 3 Summary of hepatitis B virus and alcohol induced reactive oxygen species effects on chronic liver disease and antioxidant’s protective effects. HBV: Hepatitis B virus; HBx: Hepatitis B virus X protein; VDAC3: Voltage-dependent anion channel 3; ROS: Reactive oxygen species; HSCs: Hepatic stellate cells; STAT-3: Transducer and activator of transcription 3; NF-κB: Nuclear factor κB; MAPK: Mitogen-activated protein kinase; PI3K: Phosphatidylinositol 3-kinase; CLD: Chronic liver disease; HCA: Hepatocellular adenoma; HCC: Hepatocellular carcinoma.