Role of Mitochondria in the Aging Process
R.S. Sohal
Department of Molecular Pharmacology and Toxicology
University of Southern California
Los Angeles, CA 90089-9121
An increasing amount of evidence suggests that mitochondria contribute
to the aging process both directly and indirectly. The direct role
stems from the utilization of oxygen and the consequent generation of
reactive oxygen species (ROS), which cause molecular oxidative damage.
Accumulation of such damage can be suggested to constitute the basis
for senescence-associated physiological attrition. The rates of
mitochondrial O2-/H2O2 increase with age probably due to the
corresponding elevation in the severity of oxidative damage to
mitochondria. The rates of mitochondrial O2-/H2O2 generation are also
inversely related to maximum life span (MLS) of different species.
Oxidative damage to mitochondria increases with age and accrues
inversely in relation to the MLS of different species. Experimental
regimens such as caloric restriction and others, that induce
hypometabolism and extend life span, also cause an attenuation in the
rate of mitochondrial O2-/H2O2 generation and damage. Mitochondria
contribute to aging indirectly by being the targets of ROS generated by
them. Such damage causes a decrease in mitochondrial respiratory
efficiency and an increase in their rate of ROS generation. Oxidative
damage to selective mitochondrial proteins and DNA can have global
effect on cellular physiology. It can thus be hypothesized that
mitochondria may act as one of the main determinants of the rate of
aging.
Key words:
mitochondria, aging, oxidative stress, oxidative damage
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