الفهرس 
Introduction and Aim of the workOnly 14 pages are availabe for public view
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Abstract
Cellular senesence, a process similar to apoptosis, induces irreversible growth arrest. Cells remain viable but display characteristic changes in their morphology, physiology and gene expression, and are unable to divide. Aging is a natural, complex, and multifactorial biologic process. Many of the studies conducted on cultured human cells and animals have revealed that aging is associated with impairment of bioenergetic functions, increased oxidative stress, attenuated ability to respond to stresses, and increased risk of contracting cancers and age-associated diseases. Most of these characteristics and phenomena gradually occur in advanced age in organs and tissue cells, which are usually correlated with mitochondrial ROS production, oxidative damage, accumulation of mtDNA mutations, mitochondrial dysfunction, activation of apoptosis necrosis, and altered expression of specific clusters of genes. During aging the expression levels of the genes that increase normally in response to DNA damage and oxidative stress are increased, whereas those involved in energy metabolism, biosynthesis, and protein turnover are decreased. Interestingly, it has been shown that caloric restriction can reverse or retard these changes in the gene expression during aging, extend life span, slow down aging associated physiologic changes, and reduce cancer incidence in rodents and primates. These findings suggest that modulating the rate of energy metabolism may bring about changes in the redox status, mitochondrial function, and genomic integrity of animal cells.