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Effects of Ascorbic and Dehydroascorbic Acids on Apoptotic Cell Death in Hippocampal Slice Culture

Authors
 Kim EJ  ;  Won R  ;  Lee KH  ;  Kim UJ  ;  Shim I  ;  Lee HJ  ;  Lee BH 
Citation
 EXPERIMENTAL NEUROBIOLOGY, Vol.17(1) : 25-31, 2008 
Journal Title
EXPERIMENTAL NEUROBIOLOGY
ISSN
 1226-2560 
Issue Date
2008
MeSH
Animals ; Antioxidants/administration & dosage ; Apoptosis/drug effects ; Ascorbic Acid/administration & dosage* ; Dehydroascorbic Acid/administration & dosage ; Dose-Response Relationship, Drug ; Hippocampus/cytology* ; Hippocampus/drug effects ; Hippocampus/metabolism* ; In Vitro Techniques ; Neurons/cytology* ; Neurons/drug effects ; Neurons/metabolism* ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism*
Keywords
Anti-oxidants ; Ascorbic acid ; Dehydroascorbic acid ; Kainic acid ; Reactive oxygen species ; Organotypic hippocampal slice culture
Abstract
Ascorbic acid (AA) and dehydroascorbic acid (DHA) are known to have protective effects in experimental central nerve system disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures (OHSC). Protective effects of AA and DHA on KA-induced cell death were evaluated by analyzing caspase-3. In addition, to determine if the prooxidant effect of AA is related to iron, the effect of AA on cell death was examined using desferrioxamine (DFO), an iron chelator. After 12h-KA treatment, significant delayed neuronal death was detected in CA3 region, but not in CA1. The AA (500 micrometer) and DHA (100 and 500 micrometer) pretreatments significantly prevented cell death by inhibiting caspase-3 activation in CA3 region. In the concentration of 1,000 micrometer, however, AA pretreatment might have prooxidant effect, but AA-induced oxidative reaction is mainly not related to transition metal ions. These data showed that the pretreatments of intermediate-dose AA and DHA protected KA-induced neuronal damage in OHSCs and co-pretreatment of AA and DFO did not affect cell death except for a few cases. These data suggest that both AA and DHA pretreatment have antioxidant or prooxidant effect depending on doses treated on KA-induced neuronal injury and the possible prooxidant effect of AA may not depend on the Fenton reaction
DOI
10.1016/j.bbrc.2007.11.050
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Kyung Hee(이경희)
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/107166
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