Abstract
Mitochondria are a major source of intracellular reactive oxygen species (ROS), the production of which increases with age. These organelles are also targets of oxidative damage. The deleterious effects of ROS may be responsible for impairment of mitochondrial function observed during various pathophysiological states associated with oxidative stress and aging. An important factor for protein maintenance in the presence of oxidative stress is enzymatic reversal of oxidative modifications and/or protein degradation. Failure of these protein maintenance systems is likely a critical component of the aging process. Mitochondrial matrix proteins are sensitive to oxidative inactivation and oxidized proteins are known to accumulate during aging. The ATP-stimulated mitochondrial Lon protease is a highly conserved protease found in prokaryotes and the mitochondrial compartment of eukaryotes and is believed to play an important role in the degradation of oxidized mitochondrial matrix proteins. Age-dependent declines in the activity and regulation of this proteolytic system may underlie accumulation of oxidatively modified and dysfunctional protein and loss in mitochondrial viability.
Original language | English (US) |
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Pages (from-to) | 653-657 |
Number of pages | 5 |
Journal | Experimental Gerontology |
Volume | 41 |
Issue number | 7 |
DOIs | |
State | Published - Jul 2006 |
Keywords
- Aging
- Ischemia-reperfusion
- Lon protease
- Mitochondrial protein degradation
- Oxidative stress
ASJC Scopus subject areas
- Biochemistry
- Aging
- Molecular Biology
- Genetics
- Endocrinology
- Cell Biology