Live now--pay by ageing: high performance mitochondrial activity in youth and its age-related side effects

Exp Physiol. 2003 Jan;88(1):167-74. doi: 10.1113/eph8802510.

Abstract

Radical oxygen species are a byproduct of normal energy metabolism in mitochondria. The short-lived radicals cause damage to their immediate surrounding, i.e. the mitochondria. While most of this damage will be removed by normal mitochondrial turnover, damage to mitochondrial DNA (mtDNA) can persist and may accumulate with age. Recent evidence indicates that mutant mtDNA molecules can accumulate within individual cells, potentially hampering mitochondrial function.

Publication types

  • Review

MeSH terms

  • Aging / genetics
  • Aging / physiology*
  • Animals
  • DNA Damage / genetics
  • DNA Damage / physiology*
  • DNA, Mitochondrial / genetics
  • DNA, Mitochondrial / physiology*
  • Energy Metabolism / physiology*
  • Humans
  • Mitochondria / genetics
  • Mitochondria / metabolism
  • Mitochondria / physiology*
  • Reactive Oxygen Species / metabolism*

Substances

  • DNA, Mitochondrial
  • Reactive Oxygen Species