Article

Oxidative stress induces apoptosis in C6 glioma cells: Involvement of mitogen-activated protein kinases and nuclear factor kappa B

Westmead Institute for Cancer Research, Westmead Millennium Institute, Darcy Road, 2145 Westmead, NSW Australia
Neurotoxicity Research (impact factor: 3.51). 04/2012; 3(4):397-409. DOI:10.1007/BF03033200 pp.397-409
Source: PubMed

ABSTRACT Excessive oxidative stress has been implicated in the induction of cell death in a variety of neurodegenerative diseases.
In the present study, hydrogen peroxide (H2O2)-induced cell death in rat C6 glioma cells was used as a model system for studying the molecular events associated with oxidative
stress-induced cell death in glial cells. We demonstrate that exposure of C6 glioma cells to H2O2 results in apoptotic cell death in a concentration-dependent manner, and caused activation of a member of the caspase-3-like
family of proteases resulting in cleavage of the DNA repair enzyme poly(ADP-ribose)polymerase, PARP. Furthermore, H2O2 induced a transient activation of the transcription factor, nuclear factor kappa B (NFkB). Pre-treatment of cells with the antioxidant N-acetyl-cysteine, (NAC), prevented both the activation of NFkB and the induction
of apoptosis by H2O2, suggesting a possible role for this transcription factor in oxidant-induced apoptosis in glial cells. Exposure of the cells
to H2O2 led to transient activation of both c-JunN-terminal kinase (JNK) and p38 kinase but has no effect on extracellular regulated kinase (ERK) activity. Inhibition of p38
by SB203580 did not protect the cells against H2O2-induced apoptosis suggesting that activation of p38 is not essential for H2O2-mediated cell death in C6 glioma cells.

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Keywords

antioxidant N-acetyl-cysteine
 
apoptotic cell death
 
C6 glioma cells
 
cell death
 
concentration-dependent manner
 
enzyme poly(ADP-ribose)polymerase
 
Excessive oxidative stress
 
extracellular
 
glial cells
 
H2O2 results
 
H2O2)-induced cell death
 
H2O2-mediated cell death
 
hydrogen peroxide
 
molecular events
 
neurodegenerative diseases
 
nuclear factor kappa B
 
possible role
 
rat C6 glioma cells
 
transcription factor
 
transient activation