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[The expression of bcl-2 and bax genes during microcystin induced liver tumorigenesis]
Zhijian Hu1, Hua Chen, Yiwei Li
1School of Public Health, Fujian Medical University, Fuzhou, 350004, China.
Objective:
To study the molecular mechanism of microcystin (MC) induced liver tumorigenesis in rats.
Methods:
The two-stage-medium-term tumorigenesis theory was applied to establish the animal model, and the effect of MC in liver tumor formation was evaluated by the Albert gamma-GT methods, and then, the immunohistochemical technique and image analysis were used to study the expression of the bcl-2 and bax genes during tumorigenesis.
Results:
(1) MC enhanced the formation of gamma-GT foci in liver (100%), which was significantly higher than the diethylnitrosamine (DEN) control group (22.22%) (P < 0.05). (2) MC decreased the expression of bax gene. The intensity and area of bax gene expression in the pure MC toxin group were 0.028 3 AODV and 0.007 3 ( micro m(2)/ micro m(2)) and in the DEN control group were 0.065 5 AODV and 0.024 4 ( micro m(2)/ micro m(2)), respectively. The intensity and areas of bax gene expression in the pure MC toxin group were significantly lower than those in the DEN control group (P < 0.05). (3) MC increased the expression of bcl-2 gene. The intensity and area of bcl-2 gene expression in the pure MC toxin group wee 0.097 7 AODV and 0.031 5 ( micro m(2)/ micro m(2)), respectively, and in the DEN control group were 0.046 0 AODV and 0.020 5 ( micro m(2)/ micro m(2)) respectively (P < 0.05).
Conclusion:
(1) MC can strongly promote liver tumorigenesis. (2) The changes of bcl-2 and bax gene expression possibly play an important role in the MC induced liver tumor formation.