Abstract
Substantial generation of oxygen-derived free radicals has been implicated in pathophysiology of ischemic brain damage. Immunoreactive mitochondrial manganese and cytosolic copper-zinc superoxide dismutases, initial and essential enzymes to scavenge superoxide radical anions, increased in the gerbil hippocampal neurons after transient forebrain ischemia. Neuronal cells responded to oxidative stress in ischemia and induced the protective mechanism to increase superoxide dismutases.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Gerbillinae
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Hippocampus / enzymology*
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Hippocampus / pathology
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Immunoblotting
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Immunohistochemistry
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Ischemic Attack, Transient / enzymology*
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Ischemic Attack, Transient / pathology
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Isoenzymes / isolation & purification
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Isoenzymes / metabolism*
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Molecular Weight
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Neurons / enzymology*
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Neurons / pathology
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Pyramidal Tracts / enzymology
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Pyramidal Tracts / pathology
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Reperfusion
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Superoxide Dismutase / isolation & purification
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Superoxide Dismutase / metabolism*
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Time Factors
Substances
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Isoenzymes
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Superoxide Dismutase