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• W2956003231 endingPage "3302" @default.
• W2956003231 startingPage "3302" @default.
• W2956003231 abstract "Mitochondrial oxidative stress accumulates with aging and age-related diseases and induces alterations in mitochondrial DNA (mtDNA) content. Since mtDNA qualitative alterations are also associated with aging, repair of mtDNA damage is of great importance. The most relevant form of DNA repair in this context is base excision repair (BER), which removes oxidized bases such as 8-oxoguanine (8-oxoG) and thymine glycol through the action of the mitochondrial isoform of the specific 8-oxoG DNA glycosylase/apurinic or apyrimidinic (AP) lyase (OGG1) or the endonuclease III homolog (NTH1). Mouse strains lacking OGG1 (OGG1−/−) or NTH1 (NTH1−/−) were analyzed for mtDNA alterations. Interestingly, both knockout strains presented a significant increase in mtDNA content, suggestive of a compensatory mtDNA replication. The mtDNA “common deletion” was not detected in either knockout mouse strain, likely because of the young age of the mice. Formamidopyrimidine DNA glycosylase (Fpg)-sensitive sites accumulated in mtDNA from OGG1−/− but not from NTH1−/− mice. Interestingly, the D-loop region was most severely affected by the absence of OGG1, suggesting that this region may be a hotspot for oxidative damage. Thus, we speculate that mtDNA alterations may send a stress message to evoke cell changes through a retrograde mitochondrial–nucleus communication." @default.
• W2956003231 created "2019-07-12" @default.
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• W2956003231 date "2019-07-05" @default.
• W2956003231 modified "2023-10-15" @default.
• W2956003231 title "Deletion of OGG1 Results in a Differential Signature of Oxidized Purine Base Damage in mtDNA Regions" @default.
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• W2956003231 doi "https://doi.org/10.3390/ijms20133302" @default.
• W2956003231 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6651574" @default.
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