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Zsurka G, Peeva V, Kotlyar A, et al. Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?. Genes (Basel). 2018;9(4)doi: 10.3390/genes9040175.
Zsurka, G., Peeva, V., Kotlyar, A., & Kunz, W. S. (2018). Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?. Genes, 9(4), . https://doi.org/10.3390/genes9040175
Zsurka, Gábor, et al. "Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?." Genes vol. 9,4 (2018). doi: https://doi.org/10.3390/genes9040175
Zsurka G, Peeva V, Kotlyar A, Kunz WS. Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?. Genes (Basel). 2018 Mar 21;9(4). doi: 10.3390/genes9040175. PMID: 29561808; PMCID: PMC5924517.
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Genes (Basel). 2018 Mar 21;9(4). doi: 10.3390/genes9040175.

Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?.

Genes

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

Affiliations

  1. Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany. [email protected].
  2. Department of Epileptology, University Bonn Medical Center, 53105 Bonn, Germany. [email protected].
  3. Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany. [email protected].
  4. Department of Biochemistry & Molecular Biology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel. [email protected].
  5. Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany. [email protected].
  6. Department of Epileptology, University Bonn Medical Center, 53105 Bonn, Germany. [email protected].

PMID: 29561808 PMCID: PMC5924517 DOI: 10.3390/genes9040175

Abstract

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.

Keywords: aging; mitochondrial DNA; oxidative stress; reactive oxygen species

Conflict of interest statement

The authors declare no conflict of interest.

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