1,4-苯醌致K562细胞线粒体功能障碍与凋亡作用

doi:10.3969/j.issn.1004-616x.2017.02.011

Abstract

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 20 μmol/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 potential and 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 20 μmol/L treatment groups decreased with the increased concentration of 1,4-BQ (P < 0.05). Production of ROS and cell apoptosis rates were elevated while mitochondrial membrane potential and the amounts of ATP were reduced. Between the 1,4-BQ 20 μmol/L exposure groups and the control group,the difference was statistically significant (P < 0.05 or P < 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.

Key words: 1,4-benzoquinone, K562 cell line, apoptosis, mitochondrial function

CLC Number:

R994.6

JIANG Xiaoyun, SUN Rongli, MAN Zhaodi, ZHANG Juan, PU Yuepu. Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2017, 29(2): 129-133.

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Induction of mitochondrial dysfunction and apoptosis by 1,4-benzoquinone in K562 cells

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