CLC number: R73-3
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2019-03-02
Cited: 0
Clicked: 4310
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",
volume="20",
number="4",
pages="310-321",
year="2019",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1800319"
}
%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
TY - JOUR
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
Abstract: 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.
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