title: Live now--pay by ageing: high performance mitochondrial activity in youth and its age-related side effects.
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.
authors.affiliation: Institut fur Biochemie Geb 26.42/03, Heinrich-Heine-Universitat Dusseldorf, Universitatstrase 1, D-40225 Dusseldorf, Germany. goetz.hofhaus@uni-duesseldorf.de
authors.forename: G
authors.initials: G
authors.lastname: Hofhaus
authors.forename: M
authors.initials: M
authors.lastname: Berneburg
authors.forename: M
authors.initials: M
authors.lastname: Wulfert
authors.forename: N
authors.initials: N
authors.lastname: Gattermann
mesh_terms: D000375:Aging / Q000235:genetics / Q000502:physiology*; D000818:Animals; D004249:DNA Damage / Q000235:genetics / Q000502:physiology*; D004272:DNA, Mitochondrial / Q000235:genetics / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D004272:DNA, Mitochondrial; D017382:Reactive Oxygen Species