Reactive oxygen species involved in the glutamate toxicity of C6 glioma cells via XC¯ antiporter system

Neuroscience ◽  
1996 ◽  
Vol 73 (1) ◽  
pp. 201-208 ◽  
Author(s):  
K. Mawatari ◽  
Y. Yasui ◽  
K. Sugitani ◽  
T. Takadera ◽  
S. Kato
Keyword(s):  
Reactive Oxygen Species ◽  
Glioma Cells ◽  
Reactive Oxygen ◽  
C6 Glioma ◽  
Glutamate Toxicity ◽  
C6 Glioma Cells ◽  
Oxygen Species

Mimosine-Induced Apoptosis in C6 Glioma Cells Requires the Release of Mitochondria-Derived Reactive Oxygen Species and p38, JNK Activation

2011 ◽  
Vol 37 (2) ◽  
pp. 417-427 ◽  
Author(s):  
Shanlou Qiao ◽  
Keiko Murakami ◽  
Qinghong Zhao ◽  
Baoling Wang ◽  
Hisao Seo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glioma Cells ◽  
Reactive Oxygen ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Oxygen Species ◽  
Induced Apoptosis ◽  
Jnk Activation

Cold atmospheric-pressure air plasma treatment of C6 glioma cells: effects of reactive oxygen species in the medium produced by the plasma on cell death

2017 ◽  
Vol 19 (2) ◽  
pp. 025503 ◽  
Author(s):  
Yuyang Wang (汪宇扬) ◽  
Cheng Cheng (程诚) ◽  
Peng Gao (高鹏) ◽  
Shaopeng Li (李少鹏) ◽  
Jie Shen (沈洁) ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Plasma Treatment ◽  
Atmospheric Pressure ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Oxygen Species ◽  
Air Plasma ◽  
Air Plasma Treatment

scholarly journals Blockage of Potassium Channel Inhibits Proliferation of Glioma Cells Via Increasing Reactive Oxygen Species

2014 ◽  
Vol 22 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Li Hu ◽  
Li-Li Li ◽  
Zhi-Guo Lin ◽  
Zhi-Chao Jiang ◽  
Hong-Xing Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Brain Glioma ◽  
Protein Levels ◽  
Glioma Cell Proliferation

The potassium (K+) channel plays an important role in the cell cycle and proliferation of tumor cells, while its role in brain glioma cells and the signaling pathways remains unclear. We used tetraethylammonium (TEA), a nonselective antagonist of big conductance K+ channels, to block K+ channels in glioma cells, and antioxidant N-acetyl-l-cysteine (NAC) to inhibit production of intracellular reactive oxygen species (ROS). TEA showed an antiproliferation effect on C6 and U87 glioma cells in a time-dependent manner, which was accompanied by an increased intracellular ROS level. Antioxidant NAC pretreatment reversed TEA-mediated antiproliferation and restored ROS level. TEA treatment also caused significant increases in mRNA and protein levels of tumor-suppressor proteins p53 and p21, and the upregulation was attenuated by pretreatment of NAC. Our results suggest that K+ channel activity significantly contributes to brain glioma cell proliferation via increasing ROS, and it might be an upstream factor triggering the activation of the p53/p21Cip1-dependent signaling pathway, consequently leading to glioma cell cycle arrest.

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