| Complex I specific increase in superoxide formation and respiration rate by PrP-null mouse brain mitochondria. | |
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MedLine Citation:
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PMID: 17999717 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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An imbalance in free radical production and removal is considered by many to be an important factor in the etiology of many degenerative diseases. Since mitochondria are a major source of free radicals, we have examined mitochondrial free radical production in relation to oxidative phosphorylation in PrP-null mice. Quantitative electron paramagnetic resonance spectroscopy revealed up to a 70% increase in superoxide production from Complex I of submitochondrial particles prepared from PrP-null mice. This was accompanied by elevated respiratory capacity through Complex I without any discernible alteration in respiratory efficiency. These differences are associated with changes in superoxide dismutase levels and defects in mitochondrial morphology, confirming previously reported results. Our results demonstrate a clear difference in free radical production and oxygen consumption by mitochondrial Complex I between PrP-null mice and wild-type controls, pointing to Complex I as a potential target for pathological change, suggesting similarities between prion-related and other neurodegenerative diseases. |
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Authors:
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Andrew W J Paterson; John C Curtis; Nikki K Macleod |
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Publication Detail:
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Type: Journal Article Date: 2007-11-12 |
Journal Detail:
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Title: Journal of neurochemistry Volume: 105 ISSN: 1471-4159 ISO Abbreviation: J. Neurochem. Publication Date: 2008 Apr |
Date Detail:
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Created Date: 2008-03-28 Completed Date: 2008-04-28 Revised Date: 2010-08-18 |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: England |
Other Details:
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Languages: eng Pagination: 177-91 Citation Subset: IM |
Affiliation:
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Centre for Integrative Physiology, Hugh Robson Building, George Square, Edinburgh, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Age Factors Animals Brain / ultrastructure* Cell Respiration / physiology Electron Spin Resonance Spectroscopy / methods Electron Transport Complex I / metabolism* Free Radicals / metabolism Mice Mice, Knockout Microscopy, Electron, Transmission / methods Mitochondria / physiology* Oxygen Consumption / physiology Prions / genetics* Submitochondrial Particles / metabolism Superoxides / metabolism* Voltage-Dependent Anion Channel 1 / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Free Radicals; 0/Prions; 11062-77-4/Superoxides; EC 1.6.-/Voltage-Dependent Anion Channel 1; EC 1.6.5.3/Electron Transport Complex I |
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