| Mouse and human cells versus oxygen. | |
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MedLine Citation:
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PMID: 12890857 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Peter J Hornsby |
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Publication Detail:
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Type: Journal Article Date: 2003-07-30 |
Journal Detail:
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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:
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Created Date: 2003-07-31 Completed Date: 2003-10-08 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 101146039 Medline TA: Sci Aging Knowledge Environ Country: United States |
Other Details:
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Languages: eng Pagination: PE21 Citation Subset: IM |
Affiliation:
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Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA. hornsby@uthscsa.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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