Theories of biological aging: genes, proteins, and free radicals

Free Radic Res. 2006 Dec;40(12):1230-8. doi: 10.1080/10715760600911303.

Abstract

Traditional categorization of theories of aging into programmed and stochastic ones is outdated and obsolete. Biological aging is considered to occur mainly during the period of survival beyond the natural or essential lifespan (ELS) in Darwinian terms. Organisms survive to achieve ELS by virtue of genetically determined longevity assuring maintenance and repair systems (MRS). Aging at the molecular level is characterized by the progressive accumulation of molecular damage caused by environmental and metabolically generated free radicals, by spontaneous errors in biochemical reactions, and by nutritional components. Damages in the MRS and other pathways lead to age-related failure of MRS, molecular heterogeneity, cellular dysfunctioning, reduced stress tolerance, diseases and ultimate death. A unified theory of biological aging in terms of failure of homeodynamics comprising of MRS, and involving genes, milieu and chance, is acquiring a definitive shape and wider acceptance. Such a theory also establishes the basis for testing and developing effective means of intervention, prevention and modulation of aging.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / genetics
  • Aging / physiology*
  • Animals
  • Cellular Senescence / physiology
  • DNA Damage
  • DNA Repair / physiology
  • Epigenesis, Genetic / physiology
  • Free Radicals / metabolism*
  • Homeostasis / physiology
  • Humans
  • Longevity / physiology
  • Models, Biological
  • Proteins / metabolism
  • RNA / metabolism

Substances

  • Free Radicals
  • Proteins
  • RNA