Source:http://linkedlifedata.com/resource/pubmed/id/10987855
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2000-10-5
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| pubmed:abstractText |
To address the role of oxidative DNA damage in focal cerebral ischemia lacking reperfusion, we investigated DNA base and strand damage in a rat model of permanent middle cerebral artery occlusion (MCAO). Contents of 8-hydroxyl-2'-deoxyguanosine (8-OHdG) and apurinic/apyrimidinic abasic sites (AP sites), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains obtained 4-72 h after MCAO. DNA single- and double-strand breaks were detected on coronal brain sections using in situ DNA polymerase I-mediated biotin-dATP nick-translation (PANT) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), respectively. Levels of 8-OHdG and AP sites were markedly elevated 16-72 h following MCAO in the frontal cortex, representing the peri-infarct region, but levels did not significantly change within the ischemic core regions of the caudateputamen and parietal cortex. PANT- and TUNEL-positive cells began to be detectable 4-8 h following MCAO in the caudate-putamen and parietal cortex and reached maximal levels at 72 h. PANT- and TUNEL-positive cells were also detected 16-72 h after MCAO in the lateral frontal cortex within the infarct border, where many cells also showed colocalization of DNA single-strand breaks and DNA fragmentation. In contrast, levels of PANT-positive cells alone were transiently increased (16 h after MCAO) in the medial frontal cortex, an area distant from the infarct zone. These data suggest that within peri-infarct brain regions, oxidative injury to nuclear DNA in the form of base and strand damage may be a significant and contributory cause of secondary expansion of brain damage following permanent focal ischemia.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0022-3042
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
75
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1716-28
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:10987855-Animals,
pubmed-meshheading:10987855-Blood Flow Velocity,
pubmed-meshheading:10987855-Brain,
pubmed-meshheading:10987855-Brain Chemistry,
pubmed-meshheading:10987855-Brain Infarction,
pubmed-meshheading:10987855-Brain Ischemia,
pubmed-meshheading:10987855-Cerebrovascular Circulation,
pubmed-meshheading:10987855-Chromosome Breakage,
pubmed-meshheading:10987855-DNA,
pubmed-meshheading:10987855-DNA Damage,
pubmed-meshheading:10987855-DNA Fragmentation,
pubmed-meshheading:10987855-Deoxyguanosine,
pubmed-meshheading:10987855-Disease Models, Animal,
pubmed-meshheading:10987855-In Situ Nick-End Labeling,
pubmed-meshheading:10987855-Infarction, Middle Cerebral Artery,
pubmed-meshheading:10987855-Male,
pubmed-meshheading:10987855-Oxidative Stress,
pubmed-meshheading:10987855-Rats,
pubmed-meshheading:10987855-Rats, Sprague-Dawley
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| pubmed:year |
2000
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| pubmed:articleTitle |
Induction of oxidative DNA damage in the peri-infarct region after permanent focal cerebral ischemia.
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| pubmed:affiliation |
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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