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Dehydroascorbic acid prevents oxidative cell death through a glutathione pathway in primary astrocytes

Authors
 Eun Joo Kim  ;  Yong Gou Park  ;  Eun Joo Baik  ;  Se Jung Jung  ;  Ran Won  ;  Taik Sang Nahm  ;  Bae Hwan Lee 
Citation
 JOURNAL OF NEUROSCIENCE RESEARCH, Vol.79(5) : 670-679, 2005 
Journal Title
 JOURNAL OF NEUROSCIENCE RESEARCH 
ISSN
 0360-4012 
Issue Date
2005
MeSH
Analysis of Variance ; Animals ; Animals, Newborn ; Astrocytes/drug effects* ; Astrocytes/physiology ; Brain/cytology* ; Cell Death/drug effects ; Cells, Cultured ; Dehydroascorbic Acid/pharmacology* ; Dose-Response Relationship, Drug ; Drug Interactions ; Glutathione/metabolism* ; Glutathione Peroxidase/metabolism ; Glutathione Reductase/metabolism ; Hydrogen Peroxide/pharmacology ; Membrane Potentials/drug effects ; Mice ; Mice, Inbred ICR ; Microscopy, Confocal/methods ; Mitochondria/drug effects ; Mitochondria/physiology ; Oxidative Stress/drug effects* ; Oxidative Stress/physiology ; Oxidoreductases/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects* ; Signal Transduction/physiology ; Time Factors
Keywords
ascorbic acid ; dehydroascorbic acid ; gluta-thione ; pentose phosphate pathway ; hydrogen peroxide
Abstract
Ascorbic acid (AA) is a well-known antioxidant. It also has pro-oxidant effects, however, in the presence of free transition metals. Because of the pro-oxidant effects of AA, dehydroascorbic acid (DHA), an oxidized form of AA, has been used as a substitute for AA. DHA has been shown recently to have a protective effect in an experimental stroke model. This study was carried out to determine if DHA has different effects from AA on hydrogen peroxide (H2O2)-induced oxidative cell death in primary astrocytes. DHA was found to prevent cell death and reverse mitochondrial dysfunction after exposure to H2O2. DHA significantly increased the glutathione peroxidase (GPx) and glutathione reductase (GR) activities 1 hr after H2O2 exposure. Moreover, DHA not only reversed the decrease in the glutathione (GSH) levels, but also significantly enhanced it by stimulating the pentose phosphate pathway (PPP) 15 hr after H2O2 exposure. DHA also reduced production of reactive oxygen species (ROS) after H2O2 exposure. In contrast, AA accelerated H2O2-induced cell death. To determine if the pro-oxidant effect of AA is related to iron, the effect of AA on cell death was examined using an iron chelator, desferrioxamine. Even though co-pretreatment with AA and desferrioxamine could abrogate the aggravating effects of AA on H2O2-induced cell death at early stages, it could not prevent H2O2-induced cell death over a 24-hr period. These results suggest that DHA has distinct effects from AA and prevent H2O2-induced cell death by increasing the GSH levels mediated by the GPx and GR activities and PPP.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/jnr.20384/abstract
DOI
10.1002/jnr.20384
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Rehabilitation Medicine (재활의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurosurgery (신경외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Eun Joo(김은주)
Nam, Taick Sang(남택상)
Park, Yong Gou(박용구)
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
Jung, Se Jung(정세정)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/147426
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