Medecine: Extension of murine life span by overexpression of catalase targeted to mitochondria

Samuel E. Schriner, Nancy J. Linford, George M. Martin, Piper Treuting, Charles E. Ogburn, Mary Emond, Pinar E. Coskun, Warren Ladiges, Norman Wolf, Holly Van Remmen, Douglas C. Wallace, Peter S. Rabinovitch

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1222 Scopus citations

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, H2O2 production and H 2O2-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.

Original languageEnglish (US)
Pages (from-to)1909-1911
Number of pages3
JournalScience
Volume308
Issue number5730
DOIs
StatePublished - Jun 24 2005

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    Schriner, S. E., Linford, N. J., Martin, G. M., Treuting, P., Ogburn, C. E., Emond, M., Coskun, P. E., Ladiges, W., Wolf, N., Van Remmen, H., Wallace, D. C., & Rabinovitch, P. S. (2005). Medecine: Extension of murine life span by overexpression of catalase targeted to mitochondria. Science, 308(5730), 1909-1911. https://doi.org/10.1126/science.1106653