pubmed-article:12142565 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0038836 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0040549 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0001758 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0679109 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0376669 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:12142565 | lifeskim:mentions | umls-concept:C0047640 | lld:lifeskim |
pubmed-article:12142565 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:12142565 | pubmed:dateCreated | 2002-7-26 | lld:pubmed |
pubmed-article:12142565 | pubmed:abstractText | Oxidative stress and excitotoxicity have been implicated in selective striatal vulnerability caused by the mitochondrial toxin, 3-nitropropionic acid (3-NP), which may simulate Huntington's disease in animals and humans. The detailed mechanism of the role of superoxide in striatal vulnerability induced by 3-NP is still unknown. The authors investigated oxidative cellular injury and DNA fragmentation after systemic 3-NP injection in wild-type (Wt) mice and mutant mice with a deficiency in manganese superoxide dismutase (MnSOD; Sod2 -/+). Furthermore, they investigated the effects of decortication after 3-NP treatment in Sod2 -/+ mice, and copper/zinc SOD (CuZnSOD) treatment in recently developed Sod2 -/+ mice that overexpress CuZnSOD (SOD1 +/- / Sod2 -/+ mice). Oxidized hydroethidine, 8-hydroxyguanosine immunoreactivity, and nitrotyrosine immunoreactivity were increased in the Sod2 -/+ mice compared with the Wt mice after 3-NP treatment (P < 0.001). Decortication completely abolished oxidative striatal damage after 3-NP treatment in the Sod2 -/+ mice. Increased CuZnSOD attenuated DNA fragmentation and striatal lesion volume after 3-NP treatment in the Sod2 -/+ mice (P < 0.001). These data suggest that production of superoxide may be a critical step to excitotoxicity and subsequent DNA fragmentation in selective striatal vulnerability after 3-NP treatment. | lld:pubmed |
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pubmed-article:12142565 | pubmed:language | eng | lld:pubmed |
pubmed-article:12142565 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12142565 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12142565 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12142565 | pubmed:month | Jul | lld:pubmed |
pubmed-article:12142565 | pubmed:issn | 0271-678X | lld:pubmed |
pubmed-article:12142565 | pubmed:author | pubmed-author:ChanPak HPH | lld:pubmed |
pubmed-article:12142565 | pubmed:author | pubmed-author:KimGyung WGW | lld:pubmed |
pubmed-article:12142565 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12142565 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:12142565 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12142565 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12142565 | pubmed:pagination | 798-809 | lld:pubmed |
pubmed-article:12142565 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12142565 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12142565 | pubmed:articleTitle | Involvement of superoxide in excitotoxicity and DNA fragmentation in striatal vulnerability in mice after treatment with the mitochondrial toxin, 3-nitropropionic acid. | lld:pubmed |
pubmed-article:12142565 | pubmed:affiliation | Department of Neurosurgery, Stanford University School of Medicine, California 94305-5487, USA. | lld:pubmed |
pubmed-article:12142565 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12142565 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12142565 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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