BACKGROUND/AIMS: Oxidative stress is known to play a role in the pathogenesis of a certain liver diseases such as alcoholic liver disease, metal storage disease, and ischemia/reperfusion injury. Recently oxidative stress(lipid peroxidation) has also been implicated in hepatic fibrosis, which is now regarded as a common response to chronic liver injury regardless of its nature. Development of fibrosis and cirrhosis are the major complications of chronic hepatitits B. So we aimed to detect lipid peroxidation in chronic hepatitis B and to investigate its potential role in the pathophysiology of the disease. METHODS: The subjects were histologically-proven 56 patients, including fatty liver(FL, n=8), healthy HBsAg carrier(n=6), chronic persistent hepatitis(CPH, n=8), mild chronic active hepatitis(CAH-m, n=10), severe CAH(CAH-s, n=16), and liver cirrhosis(LC, n=8). All patients were serologically HBsAg-positive except those with FL. Lipid peroxidation was detected in serum and liver specimen with TBARS(thiobarbituric acid-reacting substances) assay. Western blot and immunohistochemical stain of liver specimen were also performed, using polyclonal antibody against malondialdehyde (MDA). RESULTS: 1. There were no significant differences in serum TBARS levels among groups(p= 0.24). 2. The mean tissue TBARS level(nmol/g) was significantly higher in CAH-s group(175.4+ 41.5) than in other groups(FL 54.0+ 6.4, Carrier 51.1+ 15.9, CPH 63.9+ 2.9, CAH-m 68.9+ 7.9, LC 22.6+ 5.1) (p<0.05). 3. Tissue TBARS levels correlated with serum ALT levels(r=0.5934, p<0.05). 4. Western blot showed MDA bands only in CAH-s group. 5. Immunohistochemistry showed a strong MDA stain around portal and periportal area in CAH-s group, but weak or no stain in other groups. CONCLUSIONS: This study shows that lipid peroxidation can be detected in situ and commonly occurs in severe chronic hepatitis B. Oxidative stress may be related to active necroinflammatory change of the liver and contribute to the progression of the disease in chronic hepatitis B.