Increased molecular damage and heterogeneity as the basis of aging
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Suresh I.S. Rattan
Abstract
Aging at the molecular level is characterized by the progressive accumulation of molecular damage. The sources of damage act randomly through environmental and metabolically generated free radicals, through spontaneous errors in biochemical reactions, and through nutritional components. However, damage to a macromolecule may depend on its structure, localization and interactions with other macromolecules. Damage to the maintenance and repair pathways comprising homeodynamic machinery leads to age-related failure of homeodynamics, increased molecular heterogeneity, altered cellular functioning, reduced stress tolerance, diseases and ultimate death. Novel approaches for testing and developing effective means of intervention, prevention and modulation of aging involve means to minimize the occurrence and accumulation of molecular damage. Mild stress-induced hormesis by physical, biological and nutritional methods, including hormetins, represents a promising strategy for achieving healthy aging and for preventing age-related diseases.
©2008 by Walter de Gruyter Berlin New York
Artikel in diesem Heft
- Highlight: Oxidative Stress and Senescence
- Regulation of proteasome-mediated protein degradation during oxidative stress and aging
- Cellular responses to reactive oxygen species-induced DNA damage and aging
- Sirt1 protects the heart from aging and stress
- Klotho as a regulator of oxidative stress and senescence
- Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence
- Potential biomarkers of ageing
- Increased molecular damage and heterogeneity as the basis of aging
- Modulation of longevity-associated genes by estrogens or phytoestrogens
- FoxO transcription factors in oxidative stress response and ageing – a new fork on the way to longevity?
- Studies on the expression of 6S RNA from E. coli: involvement of regulators important for stress and growth adaptation
- New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.
- Regulation of the expression of components of the exocytotic machinery of insulin-secreting cells by microRNAs
- Kinetic properties of cathepsin D and BACE 1 indicate the need to search for additional β-secretase candidate(s)
Artikel in diesem Heft
- Highlight: Oxidative Stress and Senescence
- Regulation of proteasome-mediated protein degradation during oxidative stress and aging
- Cellular responses to reactive oxygen species-induced DNA damage and aging
- Sirt1 protects the heart from aging and stress
- Klotho as a regulator of oxidative stress and senescence
- Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence
- Potential biomarkers of ageing
- Increased molecular damage and heterogeneity as the basis of aging
- Modulation of longevity-associated genes by estrogens or phytoestrogens
- FoxO transcription factors in oxidative stress response and ageing – a new fork on the way to longevity?
- Studies on the expression of 6S RNA from E. coli: involvement of regulators important for stress and growth adaptation
- New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.
- Regulation of the expression of components of the exocytotic machinery of insulin-secreting cells by microRNAs
- Kinetic properties of cathepsin D and BACE 1 indicate the need to search for additional β-secretase candidate(s)