Abstract
The causes of aging and determinants of maximum lifespan in animal species are multifaceted and complex. However, a wealth of experimental data suggests that mitochondria are involved both in the aging process and in regulating lifespan. Here we outline a somatic cell depletion (SCD) model to account for correlations between: (1) mitochondrial reactive oxygen species and lifespan; (2) mitochondrial antioxidant enzymes and lifespan; (3) mitochondrial DNA mutation and lifespan and (4) cellular stress resistance and lifespan. We examine the available data from within the framework of the SCD model, in which mitochondrial dysfunction leading to cell death and gradual loss of essential somatic cells eventually contributes to the decline in physiological performance that limits lifespan. This model is useful in explaining many of the mitochondrial manipulations that alter maximum lifespan in a variety of animal species; however, there are a number of caveats and critical experiments outstanding, and these are outlined in this review.
Keywords: Mitochondria, lifespan, reactive oxygen species, superoxide dismutase, glutathione peroxidase, mtDNA, base excision repair, mutation
Current Aging Science
Title: Mitochondria, Cellular Stress Resistance, Somatic Cell Depletion and Lifespan
Volume: 2 Issue: 1
Author(s): Ellen L. Robb, Melissa M. Page and Jeffrey A. Stuart
Affiliation:
Keywords: Mitochondria, lifespan, reactive oxygen species, superoxide dismutase, glutathione peroxidase, mtDNA, base excision repair, mutation
Abstract: The causes of aging and determinants of maximum lifespan in animal species are multifaceted and complex. However, a wealth of experimental data suggests that mitochondria are involved both in the aging process and in regulating lifespan. Here we outline a somatic cell depletion (SCD) model to account for correlations between: (1) mitochondrial reactive oxygen species and lifespan; (2) mitochondrial antioxidant enzymes and lifespan; (3) mitochondrial DNA mutation and lifespan and (4) cellular stress resistance and lifespan. We examine the available data from within the framework of the SCD model, in which mitochondrial dysfunction leading to cell death and gradual loss of essential somatic cells eventually contributes to the decline in physiological performance that limits lifespan. This model is useful in explaining many of the mitochondrial manipulations that alter maximum lifespan in a variety of animal species; however, there are a number of caveats and critical experiments outstanding, and these are outlined in this review.
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Cite this article as:
Robb L. Ellen, Page M. Melissa and Stuart A. Jeffrey, Mitochondria, Cellular Stress Resistance, Somatic Cell Depletion and Lifespan, Current Aging Science 2009; 2 (1) . https://dx.doi.org/10.2174/1874609810902010012
DOI https://dx.doi.org/10.2174/1874609810902010012 |
Print ISSN 1874-6098 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-6128 |
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