rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1992-11-10
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pubmed:abstractText |
Kainic acid (KA) is a known potent neuroexcitotoxin, although the biochemical mechanism producing its underlying neurotoxic effect is not quite clear. Histopathological examination of gerbil brains 24 h after systemic injection of KA revealed severe neuronal lesions in different regions of the brain, especially the cerebellar and hippocampal areas. We have detected free radical formation in the brain 1 h after KA administration by using an in vivo spin trapping technique. We have also observed increased lipid peroxidation in the brain after KA-treatment by analyzing thiobarbituric acid reactive substances and conjugated diene formation. Diminished brain specific (Na+, K+)-ATPase activity was also found 2 h after KA injection and persisted to 24 h. It is possible that the free radical reaction is a primary cause of neuronal degeneration after KA administration.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1044-7393
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
51-63
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:1326973-Animals,
pubmed-meshheading:1326973-Brain Chemistry,
pubmed-meshheading:1326973-Free Radicals,
pubmed-meshheading:1326973-Gerbillinae,
pubmed-meshheading:1326973-Histocytochemistry,
pubmed-meshheading:1326973-Kainic Acid,
pubmed-meshheading:1326973-Lipid Peroxidation,
pubmed-meshheading:1326973-Malondialdehyde,
pubmed-meshheading:1326973-Nervous System Diseases,
pubmed-meshheading:1326973-Neurons,
pubmed-meshheading:1326973-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:1326973-Synaptosomes,
pubmed-meshheading:1326973-Thiobarbituric Acid Reactive Substances
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pubmed:year |
1992
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pubmed:articleTitle |
The biochemical mechanisms of the excitotoxicity of kainic acid. Free radical formation.
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pubmed:affiliation |
Department of Pharmacology, University of Missouri, Columbia 65212.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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