Abstract: Objective To explore the expression and significance of PRX2 and AKR1B10 during chemically induced hepatocar-cinogenesis in mice. Methods Primary hepatocellular carcinoma（HCC）was induced in 60 C57BL/6J mice by exposing them to a combination of diethylnitrosamines（DEN），carbon tetrachloride（CCl₄）and ethanol. Another group of 30 mice received no drugs and served as a negative control.Mice were killed on weeks 4，8，12，16 and 20 and tissue samples were harvested for staining with hematoxylin and eosin.Samples were also analyzed by QPT-PCR and immunohistochemistry to detect changes in PRX2 and AKR1B10 mRNA and protein. Results In mice with chemically induced HCC，toxic hepatitis and acute hepatocellular necrosis were observed by week 4.By week 8，hepatocellular necrosis had gotten worse and liver fibrosis was detectable.Atypical hyperplasia was observable by week 12，pseudolobule by week 16 and hepatocellular carcinoma by week 20.Expression of PRX2 and AKR1B10 was significantly higher in the HCC animals than in control animals from week 4 to 20（P<0.05），and levels continued to increase with time.Levels were significantly higher in the HCC animals by week 20 than before chemical induction of HCC（P<0.05）.Expres-sion of PRX2 mRNA positively correlated with that of AKR1B10 mRNA（r=0.674，P=0.05）. Conclusion Overexpression of PRX2 and AKR1B10 may be early events during chemically induced hepatocarcinogenesis in mice and may promote hepatocarcinogenesis.

Key words: Liver neoplasm, Hepatocarcinogenesis in mice, C57BL/6J mice, PRX2, AKR1B10