癌变·畸变·突变2017，Vol.29Issue(2)：129-133,5.DOI:10.3969/j.issn.1004-616x.2017.02.011
1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用
Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells
摘要
Abstract
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.关键词
1,4-苯醌/K562细胞系/细胞凋亡/线粒体功能Key words
1/4-benzoquinone/K562 cell line/apoptosis/mitochondrial function分类
医药卫生引用本文复制引用
蒋小云,孙蓉丽,满招娣,张娟,浦跃朴..1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用[J].癌变·畸变·突变,2017,29(2):129-133,5.基金项目
江苏省普通高校研究生科研创新计划项目(SJZZ15-0024) （SJZZ15-0024）
国家自然科学基金项目(81373034,81573120) （81373034,81573120）
