Abstract
The oxidative stress theory of aging, linking reactive oxygen species (ROS) to aging, has been accepted for more than 60 years, and numerous studies have associated ROS with various age-related diseases. A more precise version of the theory specifies that mitochondrial oxidative stress is a direct cause of aging. The naked mole rat, a unique animal with exceptional longevity (32 years in captivity), appears to be an ideal model to study successful aging and the role of ROS in this process. Several studies in the naked mole rat have shown that these animals exhibit a remarkable resistance to oxidative stress. At low concentrations, ROS serve as second messengers, and these important intracellular signalling functions are crucial for the regulation of cellular processes. In this review, we examine the literature on ROS and their functions as signal transducers. We focus specifically on the longest-lived rodent, the naked mole rat, which is a perfect example of the paradox of living an exceptionally long life with slow aging despite high levels of oxidative damage from a young age.
Highlights
Aging is defined as a progressive decline in physiological function that leads to decreased reproductive rate and increased mortality
The free radical theory of aging (FRTA) is based on the hypothesis that dysfunctions observed during aging and a range of age-associated pathologies are due to the accumulation of oxidative damage to biological macromolecules (e.g., DNA damage, lipid peroxidation, and nonrepairable protein oxidation) by reactive oxygen and nitrogen species [1, 2]
Data supporting the FRTA and the mitochondrial free radical theory of aging (MFRTA) theories come from many studies that have shown that the production of reactive oxygen species (ROS) and oxidative damage accumulate with age [7,8,9,10]
Summary
Aging is defined as a progressive decline in physiological function that leads to decreased reproductive rate and increased mortality. The free radical theory of aging (FRTA) is based on the hypothesis that dysfunctions observed during aging and a range of age-associated pathologies are due to the accumulation of oxidative damage to biological macromolecules (e.g., DNA damage, lipid peroxidation, and nonrepairable protein oxidation) by reactive oxygen and nitrogen species [1, 2]. Data supporting the FRTA and the MFRTA theories come from many studies that have shown that the production of ROS and oxidative damage accumulate with age [7,8,9,10]. In. Oxidative Medicine and Cellular Longevity agreement with the MFRTA, several studies showed that some nutritional interventions (caloric, protein, or methionine restriction but not glucose or lipid restriction) that increase longevity in rodents decrease the rate of mitochondrial ROS production in several different tissues [24,25,26,27,28,29]
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