is there still any role for oxidative stress in mitochondrial dna-dependent aging?

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ID: 258456
2018
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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.
Reference Key
zsurka2018genesis Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Gábor Zsurka;Viktoriya Peeva;Alexander Kotlyar;Wolfram S. Kunz
Journal thermal science and engineering progress
Year 2018
DOI
10.3390/genes9040175
URL
http://www.mdpi.com/2073-4425/9/4/175
Keywords
aging reactive oxygen species mitochondrial dna

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