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

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...

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Veröffentlicht in:	Experimental physiology 2003-01, Vol.88 (1), p.167-174
Hauptverfasser:	Hofhaus, G., Berneburg, M., Wulfert, M., Gattermann, N.
Format:	Artikel
Sprache:	eng
Schlagworte:	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 Special Review Series - Biogenesis and Physiological Adaptation of Mitochondria
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Beschreibung
Zusammenfassung:	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. Experimental Physiology (2003) 88.1, 167-174.
ISSN:	0958-0670 1469-445X
DOI:	10.1113/eph8802510