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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1997-4-7
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pubmed:abstractText |
Parkinson's disease may be linked to defects in mitochondrial function. Mitochondrially transformed cells (cybrids) were created from Parkinson's disease patients or disease-free controls. Parkinson's disease cybrids had 26% less complex I activity, but maintained comparable basal calcium and energy levels. Parkinson's disease cybrids recovered from a carbachol-induced increase in cytosolic calcium 53% more slowly than controls even with lanthanum and thapsigargin blockade. Inhibition of complex I with the Parkinson's disease-inducing metabolite 1-methyl-4-phenylpyridinium (MPP+) similarly reduced the rate of recovery after carbachol. This MPP(+)-induced reduction in recovery rates was much more pronounced in control cybrids than in Parkinson's disease cybrids. Parkinson's disease cybrids had less carbonyl cyanide m-chlorophenylhydrazone-releasable calcium. Bypassing complex I with succinate partially restored Parkinson's disease cybrid, and MPP+ suppressed control cybrid recovery rates. The subtle alteration in calcium homeostasis of Parkinson's disease cybrids may reflect an increased susceptibility to cell death under circumstances not ordinarily toxic.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-Methyl-4-phenylpyridinium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Carbonyl Cyanide m-Chlorophenyl...,
http://linkedlifedata.com/resource/pubmed/chemical/Dopamine Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Ionophores
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1221-33
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:9048769-1-Methyl-4-phenylpyridinium,
pubmed-meshheading:9048769-Aged,
pubmed-meshheading:9048769-Calcium,
pubmed-meshheading:9048769-Carbonyl Cyanide m-Chlorophenyl Hydrazone,
pubmed-meshheading:9048769-Cell Line, Transformed,
pubmed-meshheading:9048769-Cell Membrane,
pubmed-meshheading:9048769-Cytosol,
pubmed-meshheading:9048769-Dopamine Agents,
pubmed-meshheading:9048769-Endoplasmic Reticulum,
pubmed-meshheading:9048769-Energy Metabolism,
pubmed-meshheading:9048769-Female,
pubmed-meshheading:9048769-Homeostasis,
pubmed-meshheading:9048769-Humans,
pubmed-meshheading:9048769-Ionophores,
pubmed-meshheading:9048769-Kinetics,
pubmed-meshheading:9048769-Male,
pubmed-meshheading:9048769-Middle Aged,
pubmed-meshheading:9048769-Mitochondria,
pubmed-meshheading:9048769-Parkinson Disease,
pubmed-meshheading:9048769-Tumor Cells, Cultured
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pubmed:year |
1997
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pubmed:articleTitle |
Altered calcium homeostasis in cells transformed by mitochondria from individuals with Parkinson's disease.
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pubmed:affiliation |
Department of Neurological Surgery, University of Virginia, Charlottesville 22908, USA.
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pubmed:publicationType |
Journal Article
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