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Mitochondrial oxidative stress and mammalian healthspan
Journal article   Peer reviewed

Mitochondrial oxidative stress and mammalian healthspan

Jonathan Wanagat, Dao-Fu Dai and Peter Rabinovitch
Mechanisms of ageing and development, Vol.131(7), pp.527-535
2010
DOI: 10.1016/j.mad.2010.06.002
PMCID: PMC2933331
PMID: 20566356

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Abstract

Aging of the American society is leading to a growing need for disease-modifying interventions to treat age-related diseases and enhance healthspan. Mitochondria and mitochondrially generated reactive oxygen species appear to play a central role in these processes and are a likely target for interventions. Conventional, untargeted antioxidants have not demonstrated a clear benefit in human studies. As a result, approaches have been developed to target antioxidants specifically to mitochondria. Studies have employed a wide array of targeted molecules including antioxidant enzymes such as catalase, peroxiredoxin, superoxide dismutases and small molecular compounds which recapitulate the antioxidant activities of these enzymes. Lifespan and healthspan effects differ between interventions suggesting varied roles for specific mitochondrial reactive oxygen species and their impact on usual aging. Consistent findings in myocardial protection across various interventions support a focus on the impact of cardiac aging on healthspan. The advancement of mitochondrially targeted small-molecule antioxidants suggests the prospect of swift translation to human use.
Antioxidants Drug targeting Mitochondria Healthspan

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