期刊
NEUROBIOLOGY OF AGING
卷 29, 期 1, 页码 117-128出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2006.09.014
关键词
aging; lifespan; superoxide dismutase mimetic; free radical; oxidative stress; mitochondria; antioxidants; EPR; carboxyfullerene
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL067312] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041796, R01NS037688] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL67312-02] Funding Source: Medline
- NINDS NIH HHS [NS 41796, R01 NS041796] Funding Source: Medline
In lower organisms, such as Caenorhabditis elegans and Drosophila, many genes identified as key regulators of aging are involved in either detoxification of reactive oxygen species or the cellular response to oxidatively-damaged macromolecules. Transgenic mice have been generated to study these genes in mammalian aging, but have not in general exhibited the expected lifespan extension or beneficial behavioral effects, possibly reflecting compensatory changes during development. We administered a small-molecule synthetic enzyme superoxide dismutase (SOD) mimetic to wild-type (i.e. non-transgenic, non-senescence accelerated) mice starting at middle age. Chronic treatment not only reduced age-associated oxidative stress and mitochondrial radical production, but significantly extended lifespan. Treated mice also exhibited improved performance on the Morris water maze learning and memory task. This is to our knowledge the first demonstration that an administered antioxidant with mitochondrial activity and nervous system penetration not only increases lifespan, but rescues age-related cognitive impairment in mammals. SOD mimetics with such characteristics may provide unique complements to genetic strategies to study the contribution of oxidative processes to nervous system aging. (C) 2006 Elsevier Inc. All rights reserved.
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