Document Detail


Partial uncoupling of oxidative phosphorylation induces premature senescence in human fibroblasts and yeast mother cells.
MedLine Citation:
PMID:  17697939     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The mitochondrial theory of aging predicts that functional alterations in mitochondria leading to reactive oxygen species (ROS) production contribute to the aging process in most if not all species. Using cellular senescence as a model for human aging, we have recently reported partial uncoupling of the respiratory chain in senescent human fibroblasts. In the present communication, we address a potential cause-effect relationship between impaired mitochondrial coupling and premature senescence. Chronic exposure of human fibroblasts to the chemical uncoupler carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP) led to a temporary, reversible uncoupling of oxidative phosphorylation. FCCP inhibited cell proliferation in a dose-dependent manner, and a significant proportion of the cells entered premature senescence within 12 days. Unexpectedly, chronic exposure of cells to FCCP led to a significant increase in ROS production, and the inhibitory effect of FCCP on cell proliferation was eliminated by the antioxidant N-acetyl-cysteine. However, antioxidant treatment did not prevent premature senescence, suggesting that a reduction in the level of oxidative phosphorylation contributes to phenotypical changes characteristic of senescent human fibroblasts. To assess whether this mechanism might be conserved in evolution, the influence of mitochondrial uncoupling on replicative life span of yeast cells was also addressed. Similar to our findings in human fibroblasts, partial uncoupling of oxidative phsophorylation in yeast cells led to a substantial decrease in the mother-cell-specific life span and a concomitant incrase in ROS, indicating that life span shortening by mild mitochondrial uncoupling may represent a "public" mechanism of aging.
Authors:
Petra Stöckl; Christina Zankl; Eveline Hütter; Hermann Unterluggauer; Peter Laun; Gino Heeren; Edith Bogengruber; Dietmar Herndler-Brandstetter; Michael Breitenbach; Pidder Jansen-Dürr
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-13
Journal Detail:
Title:  Free radical biology & medicine     Volume:  43     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-16     Completed Date:  2007-10-31     Revised Date:  2011-04-06    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  947-58     Citation Subset:  IM    
Affiliation:
Institute for Biomedical Aging Research, Austrian Academy of Sciences, Rennweg 10, A-6020 Innsbruck, Austria.
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / metabolism
Aging, Premature / chemically induced,  etiology*,  metabolism
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
Cell Aging*
Cell Proliferation
Cell Respiration
Cells, Cultured
Fibroblasts / drug effects,  metabolism
Humans
Oxidative Phosphorylation* / drug effects
Reactive Oxygen Species / metabolism
Saccharomyces cerevisiae / drug effects,  metabolism
Uncoupling Agents / pharmacology
Grant Support
ID/Acronym/Agency:
S 9302-B18//Austrian Science Fund FWF
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 0/Uncoupling Agents; 370-86-5/Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; 616-91-1/Acetylcysteine

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


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