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

doi:10.1126/science.1106653

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

Department of Medicine

Research output: Contribution to journal › Article › peer-review

1361 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 language	English (US)
Pages (from-to)	1909-1911
Number of pages	3
Journal	Science
Volume	308
Issue number	5730
DOIs	https://doi.org/10.1126/science.1106653
State	Published - Jun 24 2005

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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.",

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

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T2 - Extension of murine life span by overexpression of catalase targeted to mitochondria

AU - Schriner, Samuel E.

AU - Linford, Nancy J.

AU - Martin, George M.

AU - Treuting, Piper

AU - Ogburn, Charles E.

AU - Emond, Mary

AU - Coskun, Pinar E.

AU - Ladiges, Warren

AU - Wolf, Norman

AU - Van Remmen, Holly

AU - Wallace, Douglas C.

AU - Rabinovitch, Peter S.

PY - 2005/6/24

Y1 - 2005/6/24

N2 - 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.

AB - 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.

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

Abstract

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