Is there still any role for oxidative stress in mitochondrial DNA-dependent aging?

Gábor Zsurka, Viktoriya Peeva, Alexander Kotlyar, Wolfram S. Kunz*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review


Recent deep sequencing data has provided compelling evidence that the spectrum of somatic point mutations in mitochondrial DNA (mtDNA) in aging tissues lacks G > T transversion mutations. This fact cannot, however, be used as an argument for the missing contribution of reactive oxygen species (ROS) to mitochondria-related aging because it is probably caused by the nucleotide selectivity of mitochondrial DNA polymerase γ (POLG). In contrast to point mutations, the age-dependent accumulation of mitochondrial DNA deletions is, in light of recent experimental data, still explainable by the segregation of mutant molecules generated by the direct mutagenic effects of ROS (in particular, of HO· radicals formed from H2O2 by a Fenton reaction). The source of ROS remains controversial, because the mitochondrial contribution to tissue ROS production is probably lower than previously thought. Importantly, in the discussion about the potential role of oxidative stress in mitochondria-dependent aging, ROS generated by inflammation-linked processes and the distribution of free iron also require careful consideration.

Original languageEnglish
Article number175
Issue number4
StatePublished - Apr 2018


FundersFunder number
Deutsche ForschungsgemeinschaftKU 911/21-2, ZS 99/3-2, ZS 99/3-1, KU 911/21-1
Israel Science Foundation1589/14


    • Aging
    • Mitochondrial DNA
    • Oxidative stress
    • Reactive oxygen species


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