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

1
Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany
2
Department of Epileptology, University Bonn Medical Center, 53105 Bonn, Germany
3
Department of Biochemistry & Molecular Biology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel
*
Author to whom correspondence should be addressed.
Genes 2018, 9(4), 175; https://doi.org/10.3390/genes9040175
Received: 1 February 2018 / Revised: 9 March 2018 / Accepted: 16 March 2018 / Published: 21 March 2018
(This article belongs to the Special Issue Mitochondria and Aging)
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. View Full-Text
Keywords: mitochondrial DNA; aging; reactive oxygen species; oxidative stress mitochondrial DNA; aging; reactive oxygen species; oxidative stress
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Zsurka, G.; Peeva, V.; Kotlyar, A.; Kunz, W.S. Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging? Genes 2018, 9, 175.

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