Document Detail

Complex I specific increase in superoxide formation and respiration rate by PrP-null mouse brain mitochondria.
MedLine Citation:
PMID:  17999717     Owner:  NLM     Status:  MEDLINE    
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.
Andrew W J Paterson; John C Curtis; Nikki K Macleod
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Publication Detail:
Type:  Journal Article     Date:  2007-11-12
Journal Detail:
Title:  Journal of neurochemistry     Volume:  105     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-28     Completed Date:  2008-04-28     Revised Date:  2010-08-18    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  177-91     Citation Subset:  IM    
Centre for Integrative Physiology, Hugh Robson Building, George Square, Edinburgh, UK.
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MeSH Terms
Age Factors
Brain / ultrastructure*
Cell Respiration / physiology
Electron Spin Resonance Spectroscopy / methods
Electron Transport Complex I / metabolism*
Free Radicals / metabolism
Mice, Knockout
Microscopy, Electron, Transmission / methods
Mitochondria / physiology*
Oxygen Consumption / physiology
Prions / genetics*
Submitochondrial Particles / metabolism
Superoxides / metabolism*
Voltage-Dependent Anion Channel 1 / metabolism
Reg. No./Substance:
0/Free Radicals; 0/Prions; 11062-77-4/Superoxides; EC 1.6.-/Voltage-Dependent Anion Channel 1; EC Transport Complex I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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