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目的:研究巯基供体N-乙酰半胱氨酸(NAC)和二巯丁二钠(NDMS)、抗氧化剂过氧化氢酶(CAT)和Ca~(2+)清除刘(Quin 2)对三氧化二砷诱导的三种粒系白血病细胞凋亡和端粒酶活性改变的调控作用。方法:用流式细胞仪和PCR ELISA法分别检测NAC、NDMS、CAT或Quin 2与三氧化二砷共同作用于三种粒系白血病细胞后其凋亡和端粒酶活性的变 化。结果:三氧化二砷0.6、2.7和8.1μmol/L可分别诱导急性早幼粒细胞白血病细胞株NB4,慢性粒细胞白血病细胞株K562,急性粒细胞白血病细胞株HL-60细胞发生40％-60％的凋亡,同时下调三种细胞的端粒酶活性。NAC 4mmol/L,NDMS 200μmol/L,CAT 80kU/L,Quin 220μmol/L不同程度抑制这种凋亡作用。NAC和CAT既可独立降低三种细胞的端粒酶活性,也可促进三氧化二砷对端粒酶的下调作用,而Quin 2可抑制K562和HL-60细胞中的这种下调作用。结论:三氧化二砷诱导的三种细胞的凋亡过程涉及了疏基失活、自由基的改变、细胞内Ca~(2+)浓度改变及端粒酶活性下降。NAC、NDMS、CAT及Quin 2可不同程度拮抗三氧化二砷对三种细胞的作用。
Objective: To study the sulfonium donor N-acetylcysteine (NAC) and disodium dimercaptosuccinate (NDMS), antioxidant catalase (CAT) and Ca 2+ scavenger Liu (Quin 2) on arsenic trioxide The induction of three leukemia cell apoptosis and telomerase activity regulation. METHODS: Flow cytometry and PCR ELISA were used to detect the apoptosis and telomerase activity of NAC, NDMS, CAT or Quin 2 and arsenic trioxide after they acted on three leukemia cells. RESULTS: Acute amygdala leukemia cell line NB4, chronic myelogenous leukemia cell line K562, and acute myelocytic leukemia cell line HL-60 cells were induced by 40%-60% of arsenic trioxide with 0.6, 2.7, and 8.1 μmol/L, respectively. The death, while down-regulating the telomerase activity of three kinds of cells. NAC 4 mmol/L, NDMS 200 μmol/L, CAT 80 kU/L, Quin 220 μmol/L inhibited this apoptotic effect to some extent. Both NAC and CAT can independently reduce the telomerase activity of three kinds of cells, and can also promote the down-regulation of telomerase by arsenic trioxide, while Quin 2 can inhibit this down-regulation in K562 and HL-60 cells. Conclusion: The apoptotic process of three kinds of cells induced by arsenic trioxide involves the inactivation of the hydrophobic group, the change of free radicals, the change of intracellular Ca 2+ concentration and the decrease of telomerase activity. NAC, NDMS, CAT and Quin 2 can antagonize the effects of arsenic trioxide on three kinds of cells.