Oxidative stress, mitochondrial dysfunction, and aging
- PMID: 21977319
- PMCID: PMC3184498
- DOI: 10.1155/2012/646354
Oxidative stress, mitochondrial dysfunction, and aging
Abstract
Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.
References
-
- Hayflick L. How and why we age. Experimental Gerontology. 1998;33(7-8):639–653. - PubMed
-
- Kirkwood TBL. Understanding the odd science of aging. Cell. 2005;120(4):437–447. - PubMed
-
- Harman D. Aging: a theory based on free radical and radiation chemistry. Journal of Gerontology. 1956;11(3):298–300. - PubMed
-
- Halliwell B. Reactive oxygen species in living systems: source, biochemistry, and role in human disease. American Journal of Medicine. 1991;91(3, supplement 3):14S–22S. - PubMed
-
- Chance B, Sies H, Boveris A. Hydroperoxide metabolism in mammalian organs. Physiological Reviews. 1979;59(3):527–605. - PubMed
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