Document Detail


A model of metabolic changes in respiration-deficient human cells.
MedLine Citation:
PMID:  17559336     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cells lacking aerobic metabolism because of damaged mtDNA accumulate in many postmitotic tissues in the course aging. Although being only a small fraction of cells, they might play a major role in oxidative stress affecting the whole body. However, it remains unclear how such cells, which are under normal circumstances dependent on aerobic metabolism, are able to survive for decades in vivo. Here a new model is presented that proposes a coexistence of anaerobic glycolysis and a partly reversed TCA cycle. Succinate plays a key role in the changed metabolic pathways because it has to be exported by the cell. This hypothesis supports the view that some respiration-deficient cells are able to survive permanently within the body and contribute to human aging.
Authors:
F Mathias Bollmann
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Rejuvenation research     Volume:  10     ISSN:  1549-1684     ISO Abbreviation:  Rejuvenation Res     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-07     Completed Date:  2007-11-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  101213381     Medline TA:  Rejuvenation Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  327-33     Citation Subset:  IM    
Affiliation:
Gymnasium Carolinum, Osnabrück, Germany. f.mathiasbollmann@web.de
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MeSH Terms
Descriptor/Qualifier:
Aging
Cell Aging*
Cell Respiration
DNA, Mitochondrial / metabolism*
Glycolysis
Humans
Models, Biological
Models, Theoretical
Oxidative Stress
Oxygen / metabolism*
Oxygen Consumption*
Physiological Phenomena
Succinic Acid / metabolism
Tricarboxylic Acids / chemistry
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 0/Tricarboxylic Acids; 110-15-6/Succinic Acid; 7782-44-7/Oxygen

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


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