Publication Date:
2005-05-10
Description:
To determine the role of reactive oxygen species in mammalian longevity, we generated transgenic mice that overexpress human catalase localized to the peroxisome, the nucleus, or mitochondria (MCAT). Median and maximum life spans were maximally increased (averages of 5 months and 5.5 months, respectively) in MCAT animals. Cardiac pathology and cataract development were delayed, oxidative damage was reduced, H2O2 production and H2O2-induced aconitase inactivation were attenuated, and the development of mitochondrial deletions was reduced. These results support the free radical theory of aging and reinforce the importance of mitochondria as a source of these radicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schriner, Samuel E -- Linford, Nancy J -- Martin, George M -- Treuting, Piper -- Ogburn, Charles E -- Emond, Mary -- Coskun, Pinar E -- Ladiges, Warren -- Wolf, Norman -- Van Remmen, Holly -- Wallace, Douglas C -- Rabinovitch, Peter S -- AG001751/AG/NIA NIH HHS/ -- AG13280/AG/NIA NIH HHS/ -- ES07033/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 24;308(5730):1909-11. Epub 2005 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, WA 91895, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15879174" target="_blank"〉PubMed〈/a〉
Keywords:
Aconitate Hydratase/metabolism
;
*Aging
;
Animals
;
Arteriosclerosis/pathology
;
Catalase/genetics/*metabolism
;
Cataract/pathology
;
Cell Nucleus/enzymology/metabolism
;
DNA/chemistry
;
Deoxyguanosine/*analogs & derivatives/analysis
;
Female
;
Free Radicals
;
Heart Diseases/pathology
;
Humans
;
Hydrogen Peroxide/*metabolism
;
*Longevity
;
Male
;
Mice
;
Mice, Transgenic
;
Mitochondria/enzymology/*metabolism
;
Mitochondria, Heart/enzymology/*metabolism
;
Muscle, Skeletal/chemistry
;
Myocardium/chemistry/pathology
;
Oxidation-Reduction
;
Oxidative Stress
;
Peroxisomes/enzymology
;
Reactive Oxygen Species/*metabolism
;
Reverse Transcriptase Polymerase Chain Reaction
;
Signal Transduction
;
Superoxide Dismutase/genetics/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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