Premium
Live Now ‐ Pay by Ageing: High Performance Mitochondrial Activity in Youth and its Age‐Related Side Effects
Author(s) -
Hofhaus G.,
Berneburg M.,
Wulfert M.,
Gattermann N.
Publication year - 2003
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8802510
Subject(s) - mitochondrial dna , mitochondrion , ageing , oxidative damage , energy metabolism , microbiology and biotechnology , mutant , biology , dna damage , metabolism , genetics , biochemistry , dna , endocrinology , gene , oxidative stress
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.