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目的 :探讨细胞内抗氧化剂与氧化砷 ( As2 O3 )诱导细胞凋亡的关系。方法 :采用 HL-60细胞为体外模型 ,采用流式细胞术观察不同抗氧化剂对氧化砷诱导细胞凋亡的影响。结果 :自由基清除剂超氧化物歧化酶( SOD)、过氧化氢酶 ( CAT)、维生素 C ( V-C)和巯基化合物乙酰半胱氨酸 ( CYS)可拮抗氧化砷诱导的细胞凋亡 ;砷制剂主要诱导 HL -60细胞 G2 -M期细胞凋亡 ;氧化砷对端粒酶有微弱抑制作用。结论 :砷制剂与细胞内巯基及自由基清除酶等抗氧化剂结合 ,致使酶活性下降 ,细胞抗氧化能力下降 ,可能是砷制剂诱导细胞凋亡的机理之一。
Objective: To investigate the relationship between intracellular antioxidants and arsenic trioxide (As2O3)-induced apoptosis. METHODS: HL-60 cells were used as an in vitro model. Flow cytometry was used to observe the effects of different antioxidants on apoptosis induced by arsenic trioxide. RESULTS: The free radical scavenger SOD, catalase (CAT), vitamin C (VC) and the thiol compound acetylcysteine (CYS) antagonized arsenic induced apoptosis; arsenic The preparation mainly induces apoptosis of G2-M phase cells in HL-60 cells; arsenic oxide has a weak inhibitory effect on telomerase. CONCLUSION : Arsenic is combined with antioxidants such as intracellular sulfhydryl and free radical scavenging enzymes, resulting in decreased enzyme activity and decreased cellular antioxidant capacity. This may be one of the mechanisms by which arsenic induces apoptosis.