Abstract

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, H 2 O 2 production and H 2 O 2 -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.

Keywords

CatalaseLife spanMitochondrionExtension (predicate logic)Span (engineering)Life extensionBiologyCell biologyChemistryBiochemistryGeneticsComputer scienceOxidative stressEngineeringEvolutionary biologyStructural engineering

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Publication Info

Year
2005
Type
article
Volume
308
Issue
5730
Pages
1909-1911
Citations
1701
Access
Closed

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Cite This

Samuel E. Schriner, Nancy J. Linford, George M. Martin et al. (2005). Extension of Murine Life Span by Overexpression of Catalase Targeted to Mitochondria. Science , 308 (5730) , 1909-1911. https://doi.org/10.1126/science.1106653

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DOI
10.1126/science.1106653