Background: We established a rabbit VX2 cell liver carcinoma model to evaluate effects of ischemia reperfusion (IR) on reactive oxygen species (ROS) development and liver cell apoptosis rates.
Methods: Thirty-six rabbits were divided into a control (n=6) and a VX2 hepatocellular carcinoma (HCC) model group (n=30), which received VX2 cell suspension injections into their livers. From the 30 HCC rabbits, 6 rabbits served as control without hepatic ischemia and the rest were treated with hepatic artery and portal vein clamps for 60 minutes. At 1 hour, 1 day, 3 days and 7 days of reperfusion, 6 rabbits were sacrificed and changes of catalase (CAT) and super-oxide dismutase (SOD) activities as well as apoptosis rates, measured by TUNEL assays, were compared between tumor tissues, normal tumor surrounding hepatic tissues and controls.
Results: All treated animals developed liver tumors. The CAT activity increased in both tissues 1 hour after reperfusion (P < 0.05) and dropped to low levels in the hepatocarcinoma cells at day 1 after reperfusion (P < 0.01), but increased to higher levels than the control on day 3 (P < 0.05). SOD activity decreased significantly in both tissues until day 1 after reperfusion and kept low in the hepatocarcinoma cells until day 7 (P < 0.05). The apoptosis rates after IR increased more in cancer than in normal hepatic tissues (P < 0.01).
Conclusion: Injection of VX2 tumor cell suspension into rabbit liver parenchyma achieved good results for creating a liver tumor model. IR induced apoptosis of tumor tissue and normal hepatic tissues via ROS development.
Keywords: Tumor model; catalase; ischemia reperfusion injury; liver cancer; reactive oxygen species; super-oxide dismutase.