The Free Radical Theory of Aging In Search of a Strategy for Increasing Life Span / Свободнорадикальная Теория О Старении В Поиске Стратегии Увеличить Продолжительность Жизни

Folia Medica ◽  
2013 ◽  
Vol 55 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Diana G. Ivanova ◽  
Tatyana M. Yankova

Abstract This overview is an attempt to throw a fresh look at the popular free radical theory of aging (referred to also as oxidative stress theory) which holds that the progressive decline in physiological functions is a result of accumulation of diverse deleterious changes caused by reactive oxygen species (ROS). We discuss the role of mitochondria as a major source of ROS in the cell and how these link accumulation of oxidative damage to the age-related changes in physiologic functions. The free radical theory of aging is analysed here from two different views of aging - one (the pessimistic view) that regards aging as the inevitable result of life activity the consequences of which are accumulation of errors in the genome and damage of the biomolecules, and the other (the optimistic view) which considers that it is the changes in mitochondrial pathways of apoptosis with age that cause the functional tissue changes and aging. We also discuss the possibility of delaying the aging process by appropriate diet or drug therapy, which includes also calorie restriction as a mechanism of modifying the generation of free radicals and body metabolism and thus extending lifespan as a result.

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ken Shinmura

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S416-S416
Author(s):  
Farook Jahoor ◽  
George E Taffet ◽  
Rajagopal V Sekhar

Abstract The free-radical theory of aging suggests that age-related functional decline is mediated by increases in free-radical induced oxidative-stress. Cells normally depend on antioxidants for protection against oxidative-stress. Glutathione is the most abundant endogenous intracellular antioxidant protein composed of 3 amino-acids, cysteine, glycine and glutamic-acid, and is known to be deficient in older-humans. We investigated Glutathione kinetics in older humans using a stable-isotope tracer-based approach, and found that compared to younger humans, older-humans had severe Glutathione deficiency as a result of decreased synthesis caused by limited availability of glycine and cysteine, and associated with elevated oxidative-stress. Orally supplementing glycine and cysteine (provided as N-acetylcysteine) at doses of 1.33mmol/kg/d and 0.81mmol/kg/d respectively for 2-weeks corrected their intracellular deficiency, normalized Glutathione synthesis rates and lowered oxidative-stress to levels in younger controls. These results suggest that short-term supplementation of GlyNAC at these doses can successfully correct intracellular Glutathione deficiency in older-humans.


2014 ◽  
Vol 3 (1) ◽  
Author(s):  
Jeffrey A Stuart ◽  
Lucas A Maddalena ◽  
Max Merilovich ◽  
Ellen L Robb

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