title: [Mitochondria, oxidative stress and aging].
abstract: The free radical theory of aging was defined in the 1950s. On the base of this theory, the reactive oxygen species formed in the metabolic pathways can play pivotal role in ageing. The theory was modified by defining the mitochondrial respiration as the major cellular source of reactive oxygen species and got the new name mitochondrial theory of aging. Later on the existence of a "vicious cycle" was proposed, in which the reactive oxygen species formed in the mitochondrial respiration impair the mitochondrial DNA and its functions. The formation of reactive oxygen species are elevated due to mitochondrial dysfunction. The formation of mitochondrial DNA mutations can be accelerated by this "vicious cycle", which can lead to accelerated aging. The exonuclease activity of DNA polymerase γ, the polymerase responsible for the replication of mitochondrial DNA was impaired in mtDNA mutator mouse recently. The rate of somatic mutations in mitochondrial DNA was elevated and an aging phenotype could have been observed in these mice. Surprisingly, no oxidative impairment neither elevated reactive oxygen species formation could have been observed in the mtDNA mutator mice, which may question the existence of the "vicious cycle".
authors.affiliation: Semmelweis Egyetem, Általános Orvostudományi Kar Orvosi Vegytani Molekuláris Biológiai és Patobiokémiai Intézet Budapest Pf. 260 1444 Budapesti Műszaki és Gazdaságtudományi Egyetem, Vegyészmérnöki és Biomérnöki Kar Alkalmazott Biotechnológia és Élelmiszer-tudományi Tanszék, Biokémiai és Molekuláris Biológiai Laboratórium Budapest.
authors.forename: András
authors.initials: A
authors.lastname: Szarka
authors.affiliation: Semmelweis Egyetem, Általános Orvostudományi Kar Orvosi Vegytani Molekuláris Biológiai és Patobiokémiai Intézet Budapest Pf. 260 1444.
authors.forename: Gábor
authors.initials: G
authors.lastname: Bánhegyi
authors.affiliation: Pécsi Tudományegyetem, Általános Orvostudományi Kar Biokémiai és Orvosi Kémiai Intézet, Orvosi Biokémiai Tanszék Pécs MTA PTE Nukleáris-Mitokondriális Interakciós Kutatócsoport Pécs PTE Szentágothai János Kutatóközpont Pécs.
authors.forename: Balázs
authors.initials: B
authors.lastname: Sümegi
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D016922:Cellular Senescence; D000074002:DNA Polymerase gamma; D004272:DNA, Mitochondrial / Q000378:metabolism*; D004259:DNA-Directed DNA Polymerase / Q000235:genetics*; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D051379:Mice; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D004272:DNA, Mitochondrial; D005609:Free Radicals; D017382:Reactive Oxygen Species; D000074002:DNA Polymerase gamma; D004259:DNA-Directed DNA Polymerase
keywords: aging; mitochondria; mitochondrial DNA; mitokondrium; mitokondriális DNS; reactive oxygen species; reaktív oxigénvegyületek; öregedés