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[Cancer Research 66, 2497-2499, March 1, 2006]
© 2006 American Association for Cancer Research

Reviews

Oxidative Damage and Aging: Spotlight on Mitochondria

Nancy J. Linford1, Samuel E. Schriner2 and Peter S. Rabinovitch1

1 Department of Pathology, University of Washington, Seattle, Washington and 2 Center for Molecular and Mitochondrial Medicine and Genetics, Departments of Biological Chemistry and Ecology and Evolutionary Biology, University of California, Irvine, Irvine California

Requests for reprints: Nancy J. Linford, Department of Pathology, University of Washington, Box 357705, 1959 NE Pacific Avenue, HSB K081, Seattle, WA 98195. Phone: 206-616-8201; Fax: 206-616-8271; E-mail: nantzee{at}u.washington.edu.

Whereas free radical damage has been proposed as a key component in the tissue degeneration associated with aging, there has been little evidence that free radical damage limits life span in mammals. The current research shows that overexpression of the antioxidant enzyme catalase in mitochondria can extend mouse life span. These results highlight the importance of mitochondrial damage in aging and suggest that when targeted appropriately, boosting antioxidant defenses can increase mammalian life span. (Cancer Res 2006; 66(5): 2497-9)




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P. M. Treuting, N. J. Linford, S. E. Knoblaugh, M. J. Emond, J. F. Morton, G. M. Martin, P. S. Rabinovitch, and W. C. Ladiges
Reduction of Age-Associated Pathology in Old Mice by Overexpression of Catalase in Mitochondria
J. Gerontol. A Biol. Sci. Med. Sci., August 1, 2008; 63(8): 813 - 822.
[Abstract] [Full Text] [PDF]


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Copyright © 2006 by the American Association for Cancer Research.