Document Detail


Mouse and human cells versus oxygen.
MedLine Citation:
PMID:  12890857     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mice and humans are at opposite ends of the mammalian spectrum of longevity. A major question in biology is whether this difference can be accounted for by differences in the properties of cells from these two species. A new publication from Judith Campisi's lab reports that human cells in culture are more resistant than mouse cells to the damaging effects of 20% oxygen. The greater burden of DNA damage sustained by mouse cells causes them to rapidly enter a phase of culture in which most cells enter permanent growth arrest (replicative senescence). However, some mouse cells usually escape from senescence and then grow into an immortal cell line. This never happens in human fibroblast cell cultures. Human cells also eventually enter replicative senescence in culture, but this phenomenon is caused by shortening of telomeres and not by DNA damage of the type responsible for mouse cell senescence. Human fibroblasts never spontaneously escape from senescence. This Perspective reviews differences between mouse and human cells that could account for these differences in behavior. Some evidence indicates that human cells are generally more resistant than mouse cells to oxidative damage to DNA, but more needs to be done to confirm this finding and to understand the underlying mechanisms. Whether or not there are differences in the amount of DNA damage caused by oxygen or in the early phase of repair, there may be important differences in the later consequences of DNA damage. Mouse cells appear to be able to continue to divide with DNA damage that has not been repaired or has been misrepaired, and becomes fixed in the form of chromosomal abnormalities. The checkpoints that cause cells to stop dividing when chromosomes develop abnormalities (aberrations or shortened telomeres) appear to operate more efficiently in human cells. Much more work is needed to understand the basis for these differences and the implications for aging and cancer.
Authors:
Peter J Hornsby
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Publication Detail:
Type:  Journal Article     Date:  2003-07-30
Journal Detail:
Title:  Science of aging knowledge environment : SAGE KE     Volume:  2003     ISSN:  1539-6150     ISO Abbreviation:  Sci Aging Knowledge Environ     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-07-31     Completed Date:  2003-10-08     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  101146039     Medline TA:  Sci Aging Knowledge Environ     Country:  United States    
Other Details:
Languages:  eng     Pagination:  PE21     Citation Subset:  IM    
Affiliation:
Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA. hornsby@uthscsa.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Aging / physiology*
Cells, Cultured
Chromosome Aberrations
DNA / metabolism
DNA Repair
Humans
Mice
Neoplasms / pathology
Oxidative Stress / physiology
Oxygen / physiology*
Reactive Oxygen Species / metabolism*
Species Specificity
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 7782-44-7/Oxygen; 9007-49-2/DNA

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


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