Mitochondrial oxidative stress. Physiologic consequences and potential for a role in aging
1Buck Center for Research in Aging, Novato, California 94948-0638, USA. smelov@buckcenter.org
Annals of the New York Academy of Sciences
|July 27, 2000
Summary
The free radical theory of aging is supported by studies showing reactive oxygen species (ROS) limit lifespan. Catalytic antioxidants can modulate mitochondrial ROS, potentially intervening in aging.
Area of Science:
- Biochemistry
- Genetics
- Gerontology
Background:
- The free radical theory of aging posits reactive oxygen species (ROS) contribute to age-related decline.
- Correlative data supported this theory, but rigorous testing is recent.
- Research focuses on free radical biochemistry and aging genetics.
Purpose of the Study:
- To investigate the role of endogenous ROS in aging.
- To explore the potential of catalytic antioxidants in mitigating mitochondrial oxidative stress and aging.
Main Methods:
- Utilized transgenic invertebrate models with superoxide dismutase (SOD) genes.
- Examined transgenic mice deficient in mitochondrial superoxide dismutase (SOD2).
- Investigated catalytic antioxidant intervention for mitochondrial ROS.
Main Results:
- Endogenous ROS production significantly limits lifespan in invertebrates.
- Mice lacking SOD2 exhibit early mortality, highlighting the importance of mitochondrial ROS control.
- Modulating metabolic ROS profoundly impacts lifespan.
Conclusions:
- Data from invertebrates and SOD2-deficient mice confirm ROS's role in aging.
- Catalytic antioxidants show promise in managing mitochondrial oxidative stress.
- Targeting mitochondrial ROS may offer a novel intervention strategy for aging.
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