方法：进行ACC-2细胞培养，将As₂O₃建立不同药物浓度梯度(0，1.0，2.0，4.0，8.0μmol/L)分别作用于ACC-2细胞，用Rh123染色，流式细胞仪检测8.0μmol/L As₂O₃作用前、后(24h)，ACC-2细胞的线粒体膜电位(△ψm)变化； 用多功能酶标仪进行Caspase 3活性检测。

结果：空白对照组ACC-2细胞内Rh123荧光强度最强，8.0μmol/L As₂O₃处理组ACC-2细胞内Rh123荧光强度减弱，其差异有显著性(P<0.05)； 随着As₂O₃药物浓度的增高(0， 1， 2， 4， 8μmol/L)，ACC-2细胞的Caspase 3酶活力单位逐渐增加。

结论：As₂O₃作用于ACC-2细胞，可通过降低线粒体膜电位从而引起细胞凋亡。随着As₂O₃药物浓度的增高，ACC-2细胞的Caspase 3酶活力单位逐渐增加，Caspase 3被激活，细胞可发生不可逆转的凋亡过程。

METHODS:ACC-2 cells were cultured. The As₂O₃ of different drug concentration gradients(0, 1.0, 2.0, 4.0, 8.0μmol/L)were applied to ACC-2 cells respectively. The changes in △ψm of ACC-2 cells before and after As₂O₃'s inducing(8.0μmol/L for 24h)were detected by flow cytometry with Rh123 staining. Caspase 3 activity was detected by the multifunctional microplate reader.

RESULTS: Rh123 fluorescence intensity in ACC-2 cells was strongest in the control group, while it weakened in ACC-2 cells in 8.0μmol/L As₂O₃ treatment group. The difference between two groups was significant(P<0.05). With the increase of As₂O₃ concentration(0, 1.0, 2.0, 4.0, 8.0μmol/L), Caspase 3 enzyme activity unit in ACC-2 cells gradually increased.

CONCLUSION: As₂O₃ can induce apoptosis of ACC-2 cells by reducing △ψm. Caspase 3 enzyme activity unit of ACC-2 cells gradually increases with As₂O₃ concentration increases, which results in activation of the expression of Caspase 3, and the cells' irreversible apoptosis process coming immediately.