中文摘要：

目的：研究1,4-苯醌对人慢性髓系白血病细胞（K562细胞）线粒体功能及凋亡的影响.方法：分别用终浓度为0、10、20μ,线粒体膜电位、mol/L的14-苯醌处理K562细胞24 h,用CCK-8法检测细胞活力,通过流式细胞仪检测活性氧（ROS）生成量;用三磷酸腺苷（ATP）生成量来评价线粒体功能;用PI-Annexin V双染法检测细胞的凋亡,采用分光光度法检测caspase-3酶的活性.结果：与对照组比较,1,4-苯醌10和20μmol/L染毒组K562细胞相对增殖率均降低（P均〈0.05）;随着1,4-苯醌浓度的增加,ROS生成量逐渐上升、线粒体膜电位和ATP生成量均逐渐降低、细胞的凋亡率逐渐增高,其中1,4-苯醌20μmol/L染毒组与对照组间的差异均有统计学意义（P〈0.05或P〈0.01）;caspase-3活性逐渐升高,1,4-苯醌10和20μmol/L染毒组与对照组相比差异均有统计学意义（P均〈0.01）.结论：1,4-苯醌可以诱导K562细胞ROS升高,抑制K562细胞增殖,造成线粒体功能障碍,诱导细胞凋亡升高,提示线粒体障碍在1,4-苯醌诱导K562细胞凋亡的过程中发挥了重要作用.

英文摘要：

OBJECTIVE：To determine effects of 1,4-BQ on mitochondrial dysfunction and apoptosis in human chronic myeloid leukemia cells （K562 cells）.METHODS：K562 cells were treated with 0,10,and 20μmol/L 1,4-BQ for 24 h. Cell viability was detected by CCK-8 assay,production of reactive oxygen species （ROS） was detected by flow cytometry;function of mitochondria was evaluated by measuring mitochondrial membrane potentialand adenosine triphosphate （ATP）;and caspase-3 enzyme activity was detected using spectrophotometry. RESULTS：Compared with the control,the relative growth rate of K562 cells in the 1,4-BQ 10 and 20μmol/L treatment groups decreased with the increased concentration of 1,4-BQ （P〈0.05）. Production of ROS and cell apoptosis rates were elevated whilemitochondrial membrane potential and the amounts of ATPwere reduced. Between the 1,4-BQ 20μmol/L exposure groups and the control group,the difference was statistically significant （P〈0.05 orP〈0.01）. The activity of caspase-3 was increased,and the difference was statistically significant （P〈0.01） between the control and both 1,4-BQ treatment groups. CONCLUSION：1,4-BQ induced increase of ROS in K562 cells,inhibited their proliferation and resulted in mitochondrial dysfunction and expression of apoptosis. This indicates that mitochondrial dysfunction was involved with 1,4-BQ-induction of apoptosis in K562 cells.