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Aging as a Mitochondria-Mediated Atavistic Program: Can Aging Be Switched Off?
aBelozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119992, Russia bAndrus Gerontology Center and Department of Biological Sciences, University of Southern California, Los Angeles, California 90095-1555, USA
Address for correspondence: Vladimir P. Skulachev, Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119992, Russia. skulach{at}belozersky.msu.ru
Programmed death phenomena have been demonstrated on subcellular (mitoptosis), cellular (apoptosis), and supracellular (collective apoptosis) levels. There are numerous examples of suicide mechanisms at the organismal level (phenoptosis). In yeast, it was recently shown that the death of aging cells is programmed. Many of the steps of programmed cell death are shown to be common for yeast and animals, including mammals. In particular, generation of the mitochondrial reactive oxygen species (ROS) is involved in the suicide programs. Aging of higher animals is accompanied by an increase in damage induced by mitochondrial ROS. Perhaps prevention of such damage by scavenging of mitochondrial ROS might slow down or even switch off the aging programs.
Key Words: programmed death • mitochondria • reactive oxygen species This article has been cited by other articles:
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