【摘要】 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。更多还原

【Abstract】 Objective To explore the proliferation and apoptosis effects induced by sodium arsenite and arsenic trioxide on human hepatocyte L02 and provide evidence for the paradox effects of arsenic. Methods Human hepatocyte L02 was treated by a series of concentration of sodium arsenite or arsenic trioxide,respectively. Cytotoxicity were tested by MTT assay and colony formation assay,cellular apoptosis and cell cycle were detected by flow cytometry,chromosomal breakage were measured by micronucleus test and reactive oxygen species level and GSH contents were detected with commercial kits. Results With the increase of sodium arsenite or arsenic trioxide concentrations,cellular viability,colony formation rate and GSH contents decreased; inhibition of colony formation,cellular apoptotic rate,reactive oxygen species level and frequency of micronuclei increased,and dosed cells were both arrested in G2/ M phase of cell cycle. Conclusion Both sodium arsenite and arsenic trioxide could induce oxidative stress in human hepatocyte L02 and result in chromosomal damage,apoptosis,cell cycle arrest and cellular proliferation inhibition,suggesting that oxidative stress induction might be the common molecular mechanism of malignant transformation induced by sodium arsenite and therapeutic effectsexhibited by arsenic trioxide.更多还原