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Oxidative modification of proteins during aging.

R L Levine1, E R Stadtman

  • 1Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892-0812, USA. rlevine@nih.gov

Experimental Gerontology
|August 30, 2001
PubMed
Summary

Oxidative damage to proteins, marked by carbonyl groups, increases with age. This age-related protein oxidation disrupts cellular function and is linked to lifespan in various organisms.

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Area of Science:

  • Biochemistry
  • Gerontology
  • Molecular Biology

Background:

  • Aging is associated with cellular damage.
  • Oxidative stress is a key factor in aging.
  • Reactive oxygen species damage major cellular components.

Purpose of the Study:

  • To review the role of oxidative damage to proteins during aging.
  • To focus on protein carbonyls as markers of oxidative damage.
  • To explore the relationship between protein carbonyls and lifespan.

Main Methods:

  • Review of experimental evidence on oxidative damage and aging.
  • Focus on protein carbonyls as a specific marker.
  • Analysis of lifespan-modulating factors on protein carbonyl levels.

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Main Results:

  • Reactive oxygen species target proteins, introducing carbonyl groups.
  • Protein carbonyl levels increase exponentially in the latter part of lifespan.
  • Lifespan extension reduces protein carbonyls; lifespan shortening increases them.

Conclusions:

  • Oxidative damage to proteins is a significant contributor to aging.
  • Increased protein carbonyls lead to dysfunctional proteins.
  • Elevated oxidized proteins disrupt cellular function in aging organisms.