Full Text:   <2139>

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CLC number: R73-3

On-line Access: 2019-04-01

Received: 2018-06-07

Revision Accepted: 2018-11-15

Crosschecked: 2019-03-02

Cited: 0

Clicked: 3813

Citations:  Bibtex RefMan EndNote GB/T7714


Hui Pan


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Journal of Zhejiang University SCIENCE B 2019 Vol.20 No.4 P.310-321


Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study

Author(s):  Hui Pan, Bao-hui Wang, Zhou-bin Li, Xing-guo Gong, Yong Qin, Yan Jiang, Wei-li Han

Affiliation(s):  The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):   phwbhpxc@zju.edu.cn, wang.baohui888@163.com, zjhzhwldoc@zju.edu.cn

Key Words:  Individual cell, Superoxide anion, Reactive oxygen species (ROS) dynamics, Intrinsic apoptotic pathway, Ca2+ signaling

Hui Pan, Bao-hui Wang, Zhou-bin Li, Xing-guo Gong, Yong Qin, Yan Jiang, Wei-li Han. Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study[J]. Journal of Zhejiang University Science B, 2019, 20(4): 310-321.

@article{title="Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study",
author="Hui Pan, Bao-hui Wang, Zhou-bin Li, Xing-guo Gong, Yong Qin, Yan Jiang, Wei-li Han",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study
%A Hui Pan
%A Bao-hui Wang
%A Zhou-bin Li
%A Xing-guo Gong
%A Yong Qin
%A Yan Jiang
%A Wei-li Han
%J Journal of Zhejiang University SCIENCE B
%V 20
%N 4
%P 310-321
%@ 1673-1581
%D 2019
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1800319

T1 - Mitochondrial superoxide anions induced by exogenous oxidative stress determine tumor cell fate: an individual cell-based study
A1 - Hui Pan
A1 - Bao-hui Wang
A1 - Zhou-bin Li
A1 - Xing-guo Gong
A1 - Yong Qin
A1 - Yan Jiang
A1 - Wei-li Han
J0 - Journal of Zhejiang University Science B
VL - 20
IS - 4
SP - 310
EP - 321
%@ 1673-1581
Y1 - 2019
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1800319

Objective: Reactive oxygen species (ROS) are involved in a variety of biological phenomena and serve both deleterious and beneficial roles. ROS quantification and assessment of reaction networks are desirable but difficult because of their short half-life and high reactivity. Here, we describe a pro-oxidative model in a single human lung carcinoma SPC-A-1 cell that was created by application of extracellular H2O2 stimuli. Methods: Modified microfluidics and imaging techniques were used to determine O2•− levels and construct an O2•− reaction network. To elucidate the consequences of increased O2•− input, the mitochondria were given a central role in the oxidative stress mode, by manipulating mitochondria-interrelated cytosolic Ca2+ levels, mitochondrial Ca2+ uptake, auto-amplification of intracellular ROS and the intrinsic apoptotic pathway. Results and conclusions: Results from a modified microchip demonstrated that 1 mmol/L H2O2 induced a rapid increase in cellular O2•− levels (>27 vs. >406 amol in 20 min), leading to increased cellular oxidizing power (evaluated by ROS levels) and decreased reducing power (evaluated by glutathione (GSH) levels). In addition, we examined the dynamics of cytosolic Ca2+ and mitochondrial Ca2+ by confocal laser scanning microscopy and confirmed that Ca2+ stores in the endoplasmic reticulum were the primary source of H2O2-induced cytosolic Ca2+ bursts. It is clear that mitochondria have pivotal roles in determining how exogenous oxidative stress affects cell fate. The stress response involves the transfer of Ca2+ signals between organelles, ROS auto-amplification, mitochondrial dysfunction, and a caspase-dependent apoptotic pathway.


结论:研究结果表明1 mmol/L H2O2引起细胞O2•−水平的快速增加,从而导致细胞氧化能力增加和还原能力降低.此外,研究还证实了内质网中储存的Ca2+是H2O2诱导的线粒体Ca2+爆发的主要来源.外源氧化压力反应涉及细胞器间Ca2+信号的传递、ROS自身扩增、线粒体功能紊乱和半胱天冬酶依赖性凋亡途径.线粒体在外源性氧化应激影响细胞命运方面发挥着关键作用.


Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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