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目的研究亚砷酸钠和三氧化二砷对人正常肝细胞L02增殖与凋亡效应的影响。方法分别采用亚砷酸钠和三氧化二砷处理人正常肝细胞L02,比色实验和集落形成实验检测细胞存活率,流式细胞术检测细胞凋亡和细胞周期分布,试剂盒法测定细胞内活性氧水平和谷胱甘肽含量,微核实验评价细胞染色体损伤。结果随着亚砷酸钠或三氧化二砷染毒浓度的增加,L02细胞的存活率、集落形成率和谷胱甘肽含量均下降,而集落形成抑制率、凋亡率、活性氧水平和微核率均增加,此外细胞周期都被阻滞在G2/M期。结论亚砷酸钠和三氧化二砷均能诱导人正常肝细胞L02活性氧增加和谷胱甘肽含量下降,继而引起细胞染色体损伤、细胞凋亡、细胞周期阻滞和细胞生长抑制,提示氧化应激是亚砷酸钠和三氧化二砷“致癌”与“治癌”共同的分子机制。
Objective To study the effects of sodium arsenite and arsenic trioxide on the proliferation and apoptosis of human normal liver cell line L02. Methods Human normal hepatocytes L02 were treated with sodium arsenite and arsenic trioxide, respectively. Cell viability was measured by colorimetric assay and colony formation assay. Apoptosis and cell cycle distribution were measured by flow cytometry. Reactive oxygen species And glutathione content, micronucleus test to evaluate cell chromosome damage. Results As the concentration of sodium arsenite or arsenic trioxide increased, the survival rate, colony formation rate and glutathione content of L02 cells decreased, while the colony formation inhibition rate, apoptosis rate, reactive oxygen species level and micronucleus rate All increased, furthermore the cell cycle was arrested in G2 / M phase. Conclusion Both sodium arsenite and arsenic trioxide can induce the increase of reactive oxygen species (LO2) and glutathione (GSH) in normal human hepatocytes, which in turn leads to cell chromosome damage, cell apoptosis, cell cycle arrest and cell growth inhibition, suggesting that oxidative stress is Arsenite and arsenic trioxide “carcinogenic ” and “cancer ” common molecular mechanism.