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

Kim, EJ; Park, YG; Baik, EJ; Jung, SJ; Won, R; Nahm, TS; Lee, BH
Journal of neuroscience research, 79(5):670-679, 2005
Journal Title
Journal of neuroscience research
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.
MeSH terms
Analysis of VarianceAnimalsAnimals, NewbornAstrocytes/drug effects*Astrocytes/physiologyBrain/cytology*Cell Death/drug effectsCells, CulturedDehydroascorbic Acid/pharmacology*Dose-Response Relationship, DrugDrug InteractionsGlutathione/metabolism*Glutathione Peroxidase/metabolismGlutathione Reductase/metabolismHydrogen Peroxide/pharmacologyMembrane Potentials/drug effectsMiceMice, Inbred ICRMicroscopy, Confocal/methodsMitochondria/drug effectsMitochondria/physiologyOxidative Stress/drug effects*Oxidative Stress/physiologyOxidoreductases/metabolismReactive Oxygen Species/metabolismSignal Transduction/drug effects*Signal Transduction/physiologyTime Factors
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
백, 은주
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