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Protein modification in aging
E R Stadtman1, P E Starke-Reed, C N Oliver
1Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
EXS
|January 1, 1992
Summary
Aging causes enzyme inactivation due to oxidative damage. Treating old rats with a free radical scavenger restored enzyme activity and improved short-term memory, linking oxidative stress to age-related cognitive decline.
Area of Science:
- Biochemistry
- Gerontology
- Neuroscience
Background:
- Enzymes become less active or inactive during aging.
- Oxidative stress from reactive oxygen species contributes to age-related protein damage.
Purpose of the Study:
- To investigate the link between age-dependent oxidized protein accumulation and loss of physiological function.
- To determine if reducing oxidative stress can reverse age-related biochemical and cognitive changes.
Main Methods:
- Measured levels of oxidized proteins in human fibroblasts and rat liver/brain tissues across different ages.
- Assessed enzyme activities (glutamine synthetase, glucose-6-P dehydrogenase) and protease activity in aging rats.
- Evaluated short-term memory in gerbils using the radial arm maze.
- Administered N-tert-butyl-alpha-phenylnitrone (PBN) to old rats to assess its effects on biochemical parameters and memory.
Main Results:
- Oxidized protein levels increase with age in human cells and rat tissues.
- Aging rats showed decreased enzyme activities and impaired protein degradation.
- Gerbils exhibited age-related memory loss correlating with brain biochemical changes.
- PBN treatment normalized biochemical markers and restored memory function in old rats.
Conclusions:
- Age-dependent accumulation of oxidized proteins is linked to functional decline.
- Oxidative stress plays a significant role in aging processes and cognitive impairment.
- Free radical scavenging presents a potential therapeutic strategy for age-related functional loss.