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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1991-5-24
pubmed:abstractText
The role of oxygen-derived free radicals, superoxide in particular, in the pathogenesis of neuronal cell death induced by glutamate was studied using primary culture cortical neurons from transgenic mice overexpressing human CuZn-superoxide dismutase. Primary cortical neuron cultures were developed form 15-day-old fetuses of both transgenic mice and their normal littermates. Both human CuZn-superoxide dismutase and host mouse CuZn-superoxide dismutase activities in cultured neurons were identified by native gel electrophoresis followed by nitroblue tetrazolium staining. Cultured neurons grown for 10-12 days in vitro were exposed briefly to 0.5 mM glutamate for 5 minutes, followed by biochemical and morphological examinations at 2 and 4 hours. Our data have demonstrated that glutamate neurotoxicity is significantly reduced in transgenic neurons at 2 and 4 hours following exposure to glutamate, as measured by the intracellular 3-0-methyl glucose space, the efflux of lactate dehydrogenase, and by phase-contrast and bright-field trypan blue staining. These data indicate that transgenic neurons containing two- to threefold the normal amount of CuZn-superoxide dismutase activity are protected against glutamate neurotoxicity in vitro. Our results suggest that oxidative stress play an important role in glutamate-induced neuronal swelling and toxicity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-1419
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
245-7
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Attenuation of glutamate-induced neuronal swelling and toxicity in transgenic mice overexpressing human CuZn-superoxide dismutase.
pubmed:affiliation
Department of Neurosurgery, University of California School of Medicine, San Francisco.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.