Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent 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 (RO...
Saved in:
| Published in | Genes Vol. 9; no. 4; p. 175 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
MDPI AG
21.03.2018
MDPI |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2073-4425 2073-4425 |
| DOI | 10.3390/genes9040175 |
Cover
| 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. |
|---|---|
| AbstractList | 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. 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.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. 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. 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 H 2 O 2 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. 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. |
| Author | Kotlyar, Alexander Kunz, Wolfram Zsurka, Gábor Peeva, Viktoriya |
| AuthorAffiliation | 3 Department of Biochemistry & Molecular Biology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel; s2shak@tau.ac.il 1 Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany; gabor.zsurka@ukbonn.de (G.Z.); viktoriya.peeva@ukbonn.de (V.P.) 2 Department of Epileptology, University Bonn Medical Center, 53105 Bonn, Germany |
| AuthorAffiliation_xml | – name: 2 Department of Epileptology, University Bonn Medical Center, 53105 Bonn, Germany – name: 3 Department of Biochemistry & Molecular Biology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel; s2shak@tau.ac.il – name: 1 Institute of Experimental Epileptology and Neurocognition, University Bonn Medical Center, 53105 Bonn, Germany; gabor.zsurka@ukbonn.de (G.Z.); viktoriya.peeva@ukbonn.de (V.P.) |
| Author_xml | – sequence: 1 givenname: Gábor orcidid: 0000-0002-6379-849X surname: Zsurka fullname: Zsurka, Gábor – sequence: 2 givenname: Viktoriya surname: Peeva fullname: Peeva, Viktoriya – sequence: 3 givenname: Alexander orcidid: 0000-0003-0713-6499 surname: Kotlyar fullname: Kotlyar, Alexander – sequence: 4 givenname: Wolfram orcidid: 0000-0003-1113-3493 surname: Kunz fullname: Kunz, Wolfram |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29561808$$D View this record in MEDLINE/PubMed |
| BookMark | eNptkU1PGzEQhi1ERShw67myxIVDt_X6Yze-gCKgBSkFKYSz5fXOJkaOHewNgn-PIz4UEL7Y0jzz6PXMd7TtgweEfpTkN2OS_JmBhyQJJ2UtttAuJTUrOKdie-M9QAcp3ZF8OKGEiB00oFJU5ZAMd9HkMuHpHCLgm946h0f-CU-CA9yFiK8fbat7-7AuRkgJW4__2z6YefBttNrhs6tRcQZL8C34Ho9m1s9O9tG3TrsEB6_3Hrr9ez49vSjG1_8uT0fjwvCS9kVDK8YNoy1vRadbkENNaAeUSSOh7hrJjBBAyVCYOgOV7FjFScMaZgynXLM9dPziXa6aBbQmJ4jaqWW0Cx2fVNBWfax4O1ez8KCEpFyUdRYcvQpiuF9B6tXCJgPOaQ9hlRTNUyVCcFZl9PATehdW0efvZYoTKbJxLfy5meg9ytu4M0BfABNDShE6ZWyfJxzWAa1TJVHrtarNteamX5-a3rxf4s_dsqNM |
| CitedBy_id | crossref_primary_10_1002_ana_25510 crossref_primary_10_3390_nu16142195 crossref_primary_10_3389_fnagi_2022_827900 crossref_primary_10_1016_j_heliyon_2020_e04107 crossref_primary_10_1007_s11357_020_00158_4 crossref_primary_10_1167_iovs_18_24289 crossref_primary_10_13005_bbra_3226 crossref_primary_10_1016_j_bbagen_2019_06_010 crossref_primary_10_1007_s10571_022_01265_w crossref_primary_10_1016_j_intimp_2023_110461 crossref_primary_10_31857_S0016675823110085 crossref_primary_10_1038_s41467_024_47867_4 crossref_primary_10_3389_fgene_2021_652497 crossref_primary_10_1167_iovs_61_12_3 crossref_primary_10_3390_nu11040872 crossref_primary_10_3389_fneur_2020_00881 crossref_primary_10_1098_rsbl_2020_0450 crossref_primary_10_3390_antiox10010055 crossref_primary_10_3390_biomedicines10020490 crossref_primary_10_1093_nar_gkac779 crossref_primary_10_1007_s11738_021_03326_x crossref_primary_10_1111_acel_14282 crossref_primary_10_1134_S102279542311008X crossref_primary_10_1371_journal_pone_0246114 crossref_primary_10_1007_s40572_021_00329_1 crossref_primary_10_3390_ani14192872 crossref_primary_10_3390_antiox12051087 crossref_primary_10_3390_genes14081534 crossref_primary_10_61958_NMVD5765 crossref_primary_10_1007_s10695_021_01037_1 crossref_primary_10_1093_mutage_geab003 crossref_primary_10_3390_biomedicines10051072 crossref_primary_10_1016_j_exger_2019_05_016 crossref_primary_10_1111_acel_13669 crossref_primary_10_1186_s12863_021_01005_x crossref_primary_10_3233_JPD_201981 crossref_primary_10_3390_genes11010077 crossref_primary_10_1093_toxres_tfab066 crossref_primary_10_3390_ijms22105100 crossref_primary_10_3389_fcell_2020_575645 crossref_primary_10_1155_2019_6435364 crossref_primary_10_1016_j_jbc_2023_103018 crossref_primary_10_1242_bio_033852 crossref_primary_10_3389_fcell_2022_874596 crossref_primary_10_1002_advs_202303664 |
| Cites_doi | 10.1002/j.1460-2075.1992.tb05337.x 10.1093/hmg/ddm227 10.1073/pnas.1019581108 10.1152/ajpcell.00415.2007 10.1016/0014-5793(91)80347-6 10.1016/j.neuron.2015.06.034 10.1096/fj.00-0320com 10.1016/j.bbabio.2010.03.001 10.1016/S0891-5849(02)00787-6 10.1038/ng1769 10.1042/BJ20081386 10.1371/journal.pone.0176795 10.1038/srep06569 10.1016/j.cmet.2014.07.024 10.1002/1873-3468.12956 10.1016/B978-0-12-394625-6.00002-7 10.1080/10715760600913168 10.1007/s00401-016-1561-1 10.1038/nature12474 10.18632/aging.101174 10.1016/j.mito.2011.03.007 10.1016/0022-510X(90)90006-9 10.1002/ana.24709 10.1002/bip.22680 10.1038/ncomms13548 10.1111/acel.12212 10.1073/pnas.86.20.7952 10.1038/nature02517 10.1002/ana.23568 10.1002/hep.22791 10.1016/j.cmet.2016.09.017 10.1093/nar/gkh634 10.1172/JCI19435 10.1074/jbc.M607964200 10.1073/pnas.1006586107 10.1093/hmg/11.2.133 10.1038/ng.f.94 10.1042/bj3620137 10.1038/nature13886 10.1093/jexbot/51.353.2053 10.1002/ana.20736 10.1093/hmg/ddn437 10.1042/BST0351228 10.1073/pnas.072670199 10.1093/nar/gkp091 10.1016/j.bbagen.2008.09.008 10.1016/j.cmet.2011.11.012 10.3389/fphar.2014.00019 10.1042/bj3560061 10.1074/jbc.M607965200 10.1093/hmg/ddi082 10.1146/annurev-biochem-061516-045037 10.1038/88859 10.1152/physrev.00026.2013 10.1038/ng1292-324 10.1126/science.1112125 10.1074/jbc.M310341200 10.1002/ana.22109 10.1002/bies.201100050 10.1016/j.neurobiolaging.2017.10.024 10.1093/hmg/ddu336 10.1007/s00401-012-1001-9 10.1091/mbc.e15-05-0260 10.1111/j.1742-4658.2009.07269.x 10.1371/journal.pgen.1003974 10.1016/j.bbabio.2008.03.028 10.1073/pnas.0509776102 10.1002/cbic.200600311 10.1111/j.1474-9726.2006.00209.x 10.1038/ng1292-318 10.1371/journal.pgen.1003794 10.1146/annurev.bi.61.070192.005523 10.1002/1531-8249(200011)48:5<766::AID-ANA10>3.0.CO;2-M 10.1016/j.arr.2016.04.006 10.1042/EBC20160090 10.1093/nar/27.11.2434 10.1074/jbc.273.37.23690 10.1038/ng.863 10.1016/S0027-5107(98)00066-9 10.1523/JNEUROSCI.2211-13.2013 10.1371/journal.pone.0011468 10.1016/j.cmet.2015.04.005 10.1111/j.1474-9726.2010.00581.x 10.1016/j.tig.2010.05.006 10.1177/1073858415574600 10.1074/jbc.271.35.21177 10.1038/ng.95 10.1016/S0197-4580(96)00168-6 10.1038/ng1778 10.1039/C7MT00244K 10.1016/S0960-8966(01)00332-7 10.1111/j.1471-4159.2011.07581.x |
| ContentType | Journal Article |
| Copyright | Copyright MDPI AG 2018 2018 by the authors. 2018 |
| Copyright_xml | – notice: Copyright MDPI AG 2018 – notice: 2018 by the authors. 2018 |
| DBID | AAYXX CITATION NPM 8FD 8FE 8FH ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FR3 GNUQQ HCIFZ LK8 M7P P64 PHGZM PHGZT PIMPY PKEHL PQEST PQGLB PQQKQ PQUKI PRINS RC3 7X8 5PM |
| DOI | 10.3390/genes9040175 |
| DatabaseName | CrossRef PubMed Technology Research Database ProQuest SciTech Collection ProQuest Natural Science Collection ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Local Electronic Collection Information Biological Science Collection ProQuest Central ProQuest Natural Science Collection ProQuest One Community College ProQuest Central Engineering Research Database ProQuest Central Student SciTech Premium Collection Biological Sciences ProQuest Biological Science Database (NC LIVE) Biotechnology and BioEngineering Abstracts ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef PubMed Publicly Available Content Database ProQuest Central Student Technology Research Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences Genetics Abstracts Natural Science Collection ProQuest Central Korea Biological Science Collection ProQuest Central (New) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition Biological Science Database ProQuest SciTech Collection Biotechnology and BioEngineering Abstracts ProQuest One Academic UKI Edition Engineering Research Database ProQuest One Academic ProQuest One Academic (New) MEDLINE - Academic |
| DatabaseTitleList | CrossRef MEDLINE - Academic Publicly Available Content Database PubMed |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: BENPR name: ProQuest Central url: http://www.proquest.com/pqcentral?accountid=15518 sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2073-4425 |
| ExternalDocumentID | PMC5924517 29561808 10_3390_genes9040175 |
| Genre | Journal Article Review |
| GroupedDBID | --- 53G 5VS 8FE 8FH AADQD AAFWJ AAHBH AAYXX ADBBV ADRAZ AENEX AFKRA AFZYC ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BBNVY BCNDV BENPR BHPHI CCPQU CITATION DIK EBD HCIFZ HYE IAO IPNFZ KQ8 LK8 M48 M7P MODMG M~E OK1 PGMZT PHGZM PHGZT PIMPY PROAC RIG RPM GROUPED_DOAJ NPM 8FD ABUWG AZQEC DWQXO FR3 GNUQQ P64 PKEHL PQEST PQGLB PQQKQ PQUKI PRINS RC3 7X8 PUEGO 5PM |
| ID | FETCH-LOGICAL-c412t-b2634c32d4d5fade98a02fe239c9e7fb93c55e2085c75fa69f3640b3b3cc424a3 |
| IEDL.DBID | M48 |
| ISSN | 2073-4425 |
| IngestDate | Thu Aug 21 14:07:31 EDT 2025 Fri Sep 05 03:17:06 EDT 2025 Fri Jul 25 10:37:23 EDT 2025 Wed Feb 19 02:44:18 EST 2025 Tue Jul 01 02:54:45 EDT 2025 Thu Apr 24 23:11:47 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Keywords | aging mitochondrial DNA oxidative stress reactive oxygen species |
| Language | English |
| License | https://creativecommons.org/licenses/by/4.0 Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c412t-b2634c32d4d5fade98a02fe239c9e7fb93c55e2085c75fa69f3640b3b3cc424a3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
| ORCID | 0000-0002-6379-849X 0000-0003-0713-6499 0000-0003-1113-3493 |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.3390/genes9040175 |
| PMID | 29561808 |
| PQID | 2040952457 |
| PQPubID | 2032392 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_5924517 proquest_miscellaneous_2017055436 proquest_journals_2040952457 pubmed_primary_29561808 crossref_citationtrail_10_3390_genes9040175 crossref_primary_10_3390_genes9040175 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 20180321 |
| PublicationDateYYYYMMDD | 2018-03-21 |
| PublicationDate_xml | – month: 3 year: 2018 text: 20180321 day: 21 |
| PublicationDecade | 2010 |
| PublicationPlace | Switzerland |
| PublicationPlace_xml | – name: Switzerland – name: Basel |
| PublicationTitle | Genes |
| PublicationTitleAlternate | Genes (Basel) |
| PublicationYear | 2018 |
| Publisher | MDPI AG MDPI |
| Publisher_xml | – name: MDPI AG – name: MDPI |
| References | Safdar (ref_63) 2011; 108 Itoh (ref_66) 1996; 17 Ross (ref_52) 2013; 501 Kraytsberg (ref_10) 2006; 38 Campbell (ref_81) 2012; 124 ref_58 Shoffner (ref_72) 1989; 86 Coller (ref_8) 2001; 28 ref_13 Bohr (ref_40) 2002; 32 Freudenthal (ref_43) 2015; 517 Bailey (ref_82) 2009; 37 Trifunovic (ref_14) 2004; 429 Fayet (ref_70) 2002; 12 Logan (ref_65) 2014; 13 Khrapko (ref_69) 1999; 27 Nissanka (ref_90) 2018; 592 Wiesner (ref_4) 2006; 40 Reichert (ref_36) 1978; 37 Rauen (ref_32) 2007; 8 Nido (ref_85) 2017; 63 Dutta (ref_94) 2006; 59 Alexeyev (ref_1) 2009; 276 Loeb (ref_59) 2005; 102 Kauppila (ref_3) 2017; 25 Tadi (ref_76) 2016; 27 Nido (ref_84) 2016; 7 Guliaeva (ref_37) 2006; 51 Pickrell (ref_55) 2015; 87 Fukui (ref_77) 2009; 18 Volmering (ref_49) 2016; 132 Du (ref_87) 2010; 107 Pletjushkina (ref_42) 2006; 71 Menzies (ref_12) 2009; 296 Soong (ref_6) 1992; 2 Shabalina (ref_64) 2017; 9 Petrat (ref_31) 2002; 362 Minetti (ref_44) 2015; 103 Kunz (ref_92) 2000; 48 Wallace (ref_16) 1992; 61 Genoud (ref_35) 2017; 9 Gao (ref_30) 2014; 5 Baris (ref_20) 2015; 21 DeBalsi (ref_48) 2017; 33 Henle (ref_39) 1996; 271 Sheng (ref_86) 2012; 120 Murphy (ref_26) 2009; 417 Vanderstraeten (ref_57) 1998; 273 Campbell (ref_96) 2011; 69 (ref_17) 1990; 100 Khrapko (ref_54) 2006; 5 Lin (ref_34) 2012; 71 Fellous (ref_68) 2009; 49 Koopman (ref_11) 2008; 1777 Malinska (ref_24) 2010; 1797 Sies (ref_22) 2017; 86 Hanes (ref_91) 2006; 281 Campbell (ref_95) 2012; 12 Mossmann (ref_88) 2014; 20 Payne (ref_71) 2011; 43 Krishnan (ref_73) 2008; 40 Guo (ref_75) 2010; 26 Szczepanowska (ref_2) 2017; 61 Kujoth (ref_15) 2005; 309 Zorov (ref_27) 2014; 94 Halliwell (ref_38) 1991; 281 Nekhaeva (ref_7) 2002; 99 Khrapko (ref_21) 2014; 127 Henzler (ref_28) 2000; 51 Srivastava (ref_74) 2005; 14 (ref_19) 1989; 134 ref_80 Levi (ref_29) 2009; 1790 ref_45 Vila (ref_83) 2016; 22 Lee (ref_50) 2006; 281 Vermulst (ref_60) 2008; 40 Bender (ref_9) 2006; 38 Ahlqvist (ref_62) 2012; 15 Horton (ref_5) 1992; 2 Foury (ref_56) 1992; 11 Lin (ref_89) 2002; 11 Nicholls (ref_79) 2014; 23 Graziewicz (ref_47) 2007; 16 Ross (ref_53) 2014; 4 Dai (ref_61) 2010; 9 Wang (ref_41) 1998; 400 Hoekstra (ref_46) 2016; 80 Wanrooij (ref_78) 2004; 32 Wanagat (ref_18) 2001; 15 Taylor (ref_67) 2003; 112 Claude (ref_25) 2013; 33 Petrat (ref_33) 2001; 356 Dunn (ref_51) 2011; 33 Baron (ref_93) 2007; 35 Kudin (ref_23) 2004; 279 11381261 - Nat Genet. 2001 Jun;28(2):147-50 19309719 - Hepatology. 2009 May;49(5):1655-63 1321035 - EMBO J. 1992 Jul;11(7):2717-26 11809722 - Hum Mol Genet. 2002 Jan 15;11(2):133-45 21368114 - Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4135-40 15164064 - Nature. 2004 May 27;429(6990):417-23 8702888 - J Biol Chem. 1996 Aug 30;271(35):21177-86 11943860 - Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5521-6 25409153 - Nature. 2015 Jan 29;517(7536):635-9 25955204 - Cell Metab. 2015 May 5;21(5):667-77 18948172 - Biochim Biophys Acta. 2009 Jul;1790(7):629-36 19796285 - FEBS J. 2009 Oct;276(20):5768-87 17005553 - J Biol Chem. 2006 Nov 24;281(47):36241-8 11141179 - J Exp Bot. 2000 Dec;51(353):2053-66 11156948 - FASEB J. 2001 Feb;15(2):322-32 17090418 - Free Radic Res. 2006 Dec;40(12):1284-94 25149213 - Prog Mol Biol Transl Sci. 2014;127:29-62 29281123 - FEBS Lett. 2018 Mar;592(5):728-742 21406249 - Mitochondrion. 2012 Mar;12(2):173-9 19244310 - Nucleic Acids Res. 2009 Apr;37(7):2327-35 18305478 - Nat Genet. 2008 Mar;40(3):275-9 21446022 - Ann Neurol. 2011 Mar;69(3):481-92 11978482 - Free Radic Biol Med. 2002 May 1;32(9):804-12 1497308 - Annu Rev Biochem. 1992;61:1175-212 24516391 - PLoS Genet. 2014 Feb 06;10(2):e1003974 19061483 - Biochem J. 2009 Jan 1;417(1):1-13 28944802 - Metallomics. 2017 Oct 18;9(10 ):1447-1455 25991500 - Biopolymers. 2015 Sep;103(9):491-508 9685598 - Mutat Res. 1998 May 25;400(1-2):99-115 26993140 - Acta Neuropathol. 2016 Aug;132(2):277-88 27143693 - Ageing Res Rev. 2017 Jan;33:89-104 17956319 - Biochem Soc Trans. 2007 Nov;35(Pt 5):1228-31 15181170 - Nucleic Acids Res. 2004 Jun 04;32(10):3053-64 20211146 - Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1163-70 2554297 - Proc Natl Acad Sci U S A. 1989 Oct;86(20):7952-6 14625276 - J Biol Chem. 2004 Feb 6;279(6):4127-35 20937894 - Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18670-5 24621297 - Aging Cell. 2014 Aug;13(4):765-8 16604072 - Nat Genet. 2006 May;38(5):518-20 22225879 - Cell Metab. 2012 Jan 4;15(1):100-9 20591530 - Trends Genet. 2010 Aug;26(8):340-3 18311139 - Nat Genet. 2008 Apr;40(4):392-4 16020738 - Science. 2005 Jul 15;309(5733):481-4 24986917 - Hum Mol Genet. 2014 Dec 1;23(23):6147-62 28698307 - Essays Biochem. 2017 Jul 11;61(3):325-337 22077634 - J Neurochem. 2012 Feb;120(3):419-29 10325435 - Nucleic Acids Res. 1999 Jun 1;27(11):2434-41 16365283 - Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18769-70 16842501 - Aging Cell. 2006 Jun;5(3):279-82 11079540 - Ann Neurol. 2000 Nov;48(5):766-73 19036942 - Am J Physiol Cell Physiol. 2009 Feb;296(2):C355-62 28453550 - PLoS One. 2017 Apr 28;12 (4):e0176795 28094012 - Cell Metab. 2017 Jan 10;25(1):57-71 24987008 - Physiol Rev. 2014 Jul;94(3):909-50 1303288 - Nat Genet. 1992 Dec;2(4):324-9 24086148 - PLoS Genet. 2013;9(9):e1003794 17725985 - Hum Mol Genet. 2007 Nov 15;16(22):2729-39 24227736 - J Neurosci. 2013 Nov 13;33(46):18270-6 11336636 - Biochem J. 2001 May 15;356(Pt 1):61-9 19095717 - Hum Mol Genet. 2009 Mar 15;18(6):1028-36 27874000 - Nat Commun. 2016 Nov 22;7:13548 28209927 - Aging (Albany NY). 2017 Feb 15;9(2):315-339 18435906 - Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):853-9 16909848 - Biofizika. 2006 Jul-Aug;51(4):692-7 26609070 - Mol Biol Cell. 2016 Jan 15;27(2):223-35 16392116 - Ann Neurol. 2006 Mar;59(3):478-89 2541614 - Am J Pathol. 1989 May;134(5):1167-73 11829750 - Biochem J. 2002 Feb 15;362(Pt 1):137-47 17219451 - Chembiochem. 2007 Feb 12;8(3):341-52 25761946 - Neuroscientist. 2016 Jun;22(3):266-77 20456298 - Aging Cell. 2010 Aug;9(4):536-44 24596558 - Front Pharmacol. 2014 Feb 17;5:19 14597761 - J Clin Invest. 2003 Nov;112(9):1351-60 22688405 - Acta Neuropathol. 2012 Aug;124(2):209-20 29257976 - Neurobiol Aging. 2018 Mar;63:120-127 16604074 - Nat Genet. 2006 May;38(5):515-7 23965628 - Nature. 2013 Sep 19;501(7467):412-5 1965203 - J Neurol Sci. 1990 Dec;100(1-2):14-21 26182419 - Neuron. 2015 Jul 15;87(2):371-81 21706004 - Nat Genet. 2011 Jun 26;43(8):806-10 15703189 - Hum Mol Genet. 2005 Apr 1;14(7):893-902 749453 - Acta Biol Med Ger. 1978;37(8):1167-76 17005554 - J Biol Chem. 2006 Nov 24;281(47):36236-40 9363794 - Neurobiol Aging. 1996 Nov-Dec;17(6):843-8 9726974 - J Biol Chem. 1998 Sep 11;273(37):23690-7 27315116 - Ann Neurol. 2016 Aug;80(2):301-6 16457620 - Biochemistry (Mosc). 2006 Jan;71(1):60-7 25299268 - Sci Rep. 2014 Oct 09;4:6569 28441057 - Annu Rev Biochem. 2017 Jun 20;86:715-748 12031622 - Neuromuscul Disord. 2002 Jun;12(5):484-93 1303287 - Nat Genet. 1992 Dec;2(4):318-23 22718549 - Ann Neurol. 2012 Jun;71(6):850-4 25176146 - Cell Metab. 2014 Oct 7;20(4):662-9 20628647 - PLoS One. 2010 Jul 07;5(7):e11468 1849843 - FEBS Lett. 1991 Apr 9;281(1-2):9-19 21826691 - Bioessays. 2011 Oct;33(10):742-8 |
| References_xml | – volume: 11 start-page: 2717 year: 1992 ident: ref_56 article-title: Yeast mitochondrial DNA mutators with deficient proofreading exonucleolytic activity publication-title: EMBO J. doi: 10.1002/j.1460-2075.1992.tb05337.x – volume: 16 start-page: 2729 year: 2007 ident: ref_47 article-title: The DNA polymerase γ Y955C disease variant associated with PEO and parkinsonism mediates the incorporation and translesion synthesis opposite 7,8-dihydro-8-oxo-20-deoxyguanosine publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddm227 – volume: 108 start-page: 4135 year: 2011 ident: ref_63 article-title: Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice publication-title: Proc. Natl Acad. Sci. USA doi: 10.1073/pnas.1019581108 – volume: 296 start-page: C355 year: 2009 ident: ref_12 article-title: Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects publication-title: Am. J. Physiol. Cell Physiol. doi: 10.1152/ajpcell.00415.2007 – volume: 281 start-page: 9 year: 1991 ident: ref_38 article-title: DNA damage by oxygen-derived species. Its mechanism and measurement in mammalian systems publication-title: FEBS Lett. doi: 10.1016/0014-5793(91)80347-6 – volume: 87 start-page: 371 year: 2015 ident: ref_55 article-title: Endogenous Parkin preserves dopaminergic substantia nigral neurons following mitochondrial DNA mutagenic stress publication-title: Neuron doi: 10.1016/j.neuron.2015.06.034 – volume: 15 start-page: 322 year: 2001 ident: ref_18 article-title: Mitochondrial DNA deletion mutations colocalize with segmental electron transport system abnormalities, muscle fiber atrophy, fiber splitting, and oxidative damage in sarcopenia publication-title: FASEB J. doi: 10.1096/fj.00-0320com – volume: 1797 start-page: 1163 year: 2010 ident: ref_24 article-title: Complex III-dependent superoxide production of brain mitochondria contributes to seizure-related ROS formation publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbabio.2010.03.001 – volume: 32 start-page: 804 year: 2002 ident: ref_40 article-title: Repair of oxidative DNA damage in nuclear and mitochondrial DNA, and some changes with aging in mammalian cells publication-title: Free Radic. Biol. Med. doi: 10.1016/S0891-5849(02)00787-6 – volume: 38 start-page: 515 year: 2006 ident: ref_9 article-title: High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease publication-title: Nat. Genet. doi: 10.1038/ng1769 – volume: 417 start-page: 1 year: 2009 ident: ref_26 article-title: How mitochondria produce reactive oxygen species publication-title: Biochem. J. doi: 10.1042/BJ20081386 – ident: ref_80 doi: 10.1371/journal.pone.0176795 – volume: 4 start-page: 6569 year: 2014 ident: ref_53 article-title: Maternally transmitted mitochondrial DNA mutations can reduce lifespan publication-title: Sci. Rep. doi: 10.1038/srep06569 – volume: 20 start-page: 662 year: 2014 ident: ref_88 article-title: Amyloid-β peptide induces mitochondrial dysfunction by inhibition of preprotein maturation publication-title: Cell Metab. doi: 10.1016/j.cmet.2014.07.024 – volume: 592 start-page: 728 year: 2018 ident: ref_90 article-title: Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease publication-title: FEBS Lett. doi: 10.1002/1873-3468.12956 – volume: 127 start-page: 29 year: 2014 ident: ref_21 article-title: Mitochondrial DNA mutations in aging publication-title: Prog. Mol. Biol. Transl. Sci. doi: 10.1016/B978-0-12-394625-6.00002-7 – volume: 40 start-page: 1284 year: 2006 ident: ref_4 article-title: Mitochondrial DNA damage and the aging process: Facts and imaginations publication-title: Free Radic. Res. doi: 10.1080/10715760600913168 – volume: 132 start-page: 277 year: 2016 ident: ref_49 article-title: Neuropathological signs of inflammation correlate with mitochondrial DNA deletions in mesial temporal lobe epilepsy publication-title: Acta Neuropathol. doi: 10.1007/s00401-016-1561-1 – volume: 501 start-page: 412 year: 2013 ident: ref_52 article-title: Germline mitochondrial DNA mutations aggravate ageing and can impair brain development publication-title: Nature doi: 10.1038/nature12474 – volume: 9 start-page: 315 year: 2017 ident: ref_64 article-title: Improved health-span and lifespan in mtDNA mutator mice treated with the mitochondrially targeted antioxidant SkQ1 publication-title: Aging doi: 10.18632/aging.101174 – volume: 12 start-page: 173 year: 2012 ident: ref_95 article-title: Mitochondrial changes associated with demyelination: Consequences for axonal integrity publication-title: Mitochondrion doi: 10.1016/j.mito.2011.03.007 – volume: 100 start-page: 14 year: 1990 ident: ref_17 article-title: Cytochrome c oxidase deficient fibres in the limb muscle and diaphragm of man without muscular disease: An age-related alteration publication-title: J. Neurol. Sci. doi: 10.1016/0022-510X(90)90006-9 – volume: 80 start-page: 301 year: 2016 ident: ref_46 article-title: Mitochondrial DNA mutations increase in early stage Alzheimer disease and are inconsistent with oxidative damage publication-title: Ann. Neurol. doi: 10.1002/ana.24709 – volume: 103 start-page: 491 year: 2015 ident: ref_44 article-title: Impact of thymine glycol damage on DNA duplex energetics: Correlations with lesion-induced biochemical and structural consequences publication-title: Biopolymers doi: 10.1002/bip.22680 – volume: 7 start-page: 13548 year: 2016 ident: ref_84 article-title: Defective mitochondrial DNA homeostasis in the substantia nigra in Parkinson disease publication-title: Nat. Commun. doi: 10.1038/ncomms13548 – volume: 13 start-page: 765 year: 2014 ident: ref_65 article-title: In vivo levels of mitochondrial hydrogen peroxide increase with age in mtDNA mutator mice publication-title: Aging Cell doi: 10.1111/acel.12212 – volume: 86 start-page: 7952 year: 1989 ident: ref_72 article-title: Spontaneous Kearns-Sayre/chronic external ophthalmoplegia plus syndrome associated with a mitochondrial DNA deletion: A slip-replication model and metabolic therapy publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.86.20.7952 – volume: 429 start-page: 417 year: 2004 ident: ref_14 article-title: Premature ageing in mice expressing defective mitochondrial DNA polymerase publication-title: Nature doi: 10.1038/nature02517 – volume: 71 start-page: 850 year: 2012 ident: ref_34 article-title: Somatic mitochondrial DNA mutations in early Parkinson and incidental Lewy body disease publication-title: Ann. Neurol. doi: 10.1002/ana.23568 – volume: 49 start-page: 1655 year: 2009 ident: ref_68 article-title: Locating the stem cell niche and tracing hepatocyte lineages in human liver publication-title: Hepatology doi: 10.1002/hep.22791 – volume: 25 start-page: 57 year: 2017 ident: ref_3 article-title: Mammalian mitochondria and aging: An update publication-title: Cell Metab. doi: 10.1016/j.cmet.2016.09.017 – volume: 32 start-page: 3053 year: 2004 ident: ref_78 article-title: Twinkle and POLG defects enhance age-dependent accumulation of mutations in the control region of mtDNA publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkh634 – volume: 112 start-page: 1351 year: 2003 ident: ref_67 article-title: Mitochondrial DNA mutations in human colonic crypt stem cells publication-title: J. Clin. Invest. doi: 10.1172/JCI19435 – volume: 281 start-page: 36236 year: 2006 ident: ref_50 article-title: Fidelity of the human mitochondrial DNA polymerase publication-title: J. Biol. Chem. doi: 10.1074/jbc.M607964200 – volume: 107 start-page: 18670 year: 2010 ident: ref_87 article-title: Early deficits in synaptic mitochondria in an Alzheimer’s disease mouse model publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.1006586107 – volume: 11 start-page: 133 year: 2002 ident: ref_89 article-title: High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer’s disease brain publication-title: Hum. Mol. Genet doi: 10.1093/hmg/11.2.133 – volume: 40 start-page: 275 year: 2008 ident: ref_73 article-title: What causes mitochondrial DNA deletions in human cells? publication-title: Nat. Genet. doi: 10.1038/ng.f.94 – volume: 362 start-page: 137 year: 2002 ident: ref_31 article-title: Selective determination of mitochondrial chelatable iron in viable cells with a new fluorescent sensor publication-title: Biochem. J. doi: 10.1042/bj3620137 – volume: 517 start-page: 635 year: 2015 ident: ref_43 article-title: Uncovering the polymerase induced cytotoxicity of an oxidized nucleotide publication-title: Nature doi: 10.1038/nature13886 – volume: 51 start-page: 2053 year: 2000 ident: ref_28 article-title: Transport and metabolic degradation of hydrogen peroxide in Chara corallina: Model calculations and measurements with the pressure probe suggest transport of H2O2 across water channels publication-title: J. Exp. Bot. doi: 10.1093/jexbot/51.353.2053 – volume: 59 start-page: 478 year: 2006 ident: ref_94 article-title: Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients publication-title: Ann. Neurol. doi: 10.1002/ana.20736 – volume: 18 start-page: 1028 year: 2009 ident: ref_77 article-title: Mechanisms of formation and accumulation of mitochondrial DNA deletions in aging neurons publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddn437 – volume: 35 start-page: 1228 year: 2007 ident: ref_93 article-title: Mitochondrial dysfunction in neurodegenerative disorders publication-title: Biochem. Soc. Trans. doi: 10.1042/BST0351228 – volume: 99 start-page: 5521 year: 2002 ident: ref_7 article-title: Clonally expanded mtDNA point mutations are abundant in individual cells of human tissues publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.072670199 – volume: 37 start-page: 2327 year: 2009 ident: ref_82 article-title: Mice expressing an error-prone DNA polymerase in mitochondria display elevated replication pausing and chromosomal breakage at fragile sites of mitochondrial DNA publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkp091 – volume: 1790 start-page: 629 year: 2009 ident: ref_29 article-title: The role of iron in mitochondrial function publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbagen.2008.09.008 – volume: 15 start-page: 100 year: 2012 ident: ref_62 article-title: Somatic progenitor cell vulnerability to mitochondrial DNA mutagenesis underlies progeroid phenotypes in Polg mutator mice publication-title: Cell Metab. doi: 10.1016/j.cmet.2011.11.012 – volume: 5 start-page: 19 year: 2014 ident: ref_30 article-title: Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases publication-title: Front. Pharmacol. doi: 10.3389/fphar.2014.00019 – volume: 356 start-page: 61 year: 2001 ident: ref_33 article-title: Subcellular distribution of chelatable iron: A laser scanning microscopic study in isolated hepatocytes and liver endothelial cells publication-title: Biochem. J. doi: 10.1042/bj3560061 – volume: 281 start-page: 36241 year: 2006 ident: ref_91 article-title: Incorporation and replication of 8-oxo-deoxyguanosine by the human mitochondrial DNA polymerase publication-title: J. Biol. Chem. doi: 10.1074/jbc.M607965200 – volume: 14 start-page: 893 year: 2005 ident: ref_74 article-title: Double-strand breaks of mouse muscle mtDNA promote large deletions similar to multiple mtDNA deletions in humans publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddi082 – volume: 86 start-page: 715 year: 2017 ident: ref_22 article-title: Oxidative stress publication-title: Annu. Rev. Biochem. doi: 10.1146/annurev-biochem-061516-045037 – volume: 28 start-page: 147 year: 2001 ident: ref_8 article-title: High frequency of homoplasmic mitochondrial DNA mutations in human tumors can be explained without selection publication-title: Nat. Genet. doi: 10.1038/88859 – volume: 94 start-page: 909 year: 2014 ident: ref_27 article-title: Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release publication-title: Physiol. Rev. doi: 10.1152/physrev.00026.2013 – volume: 2 start-page: 324 year: 1992 ident: ref_5 article-title: Mitochondrial DNA deletions in human brain: Regional variability and increase with advanced age publication-title: Nat. Genet. doi: 10.1038/ng1292-324 – volume: 309 start-page: 481 year: 2005 ident: ref_15 article-title: Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging publication-title: Science doi: 10.1126/science.1112125 – volume: 279 start-page: 4127 year: 2004 ident: ref_23 article-title: Characterization of superoxide-producing sites in isolated brain mitochondria publication-title: J. Biol. Chem. doi: 10.1074/jbc.M310341200 – volume: 37 start-page: 1167 year: 1978 ident: ref_36 article-title: The dependence on the extramitochondrial ATP/ADP-ratio of the oxidative phosphorylation in mitochondria isolated by a new procedure from rat skeletal muscle publication-title: Acta Biol. Med. Ger. – volume: 69 start-page: 481 year: 2011 ident: ref_96 article-title: Mitochondrial DNA deletions and neurodegeneration in multiple sclerosis publication-title: Ann. Neurol. doi: 10.1002/ana.22109 – volume: 134 start-page: 1167 year: 1989 ident: ref_19 article-title: Cytochrome-c-oxidase deficient cardiomyocytes in the human heart—An age-related phenomenon. A histochemical ultracytochemical study publication-title: Am. J. Pathol. – volume: 33 start-page: 742 year: 2011 ident: ref_51 article-title: Running on empty: Does mitochondrial DNA mutation limit replicative lifespan in yeast? publication-title: Bioessays doi: 10.1002/bies.201100050 – volume: 63 start-page: 120 year: 2017 ident: ref_85 article-title: Ultradeep mapping of neuronal mitochondrial deletions in Parkinson’s disease publication-title: Neurobiol. Aging. doi: 10.1016/j.neurobiolaging.2017.10.024 – volume: 23 start-page: 6147 year: 2014 ident: ref_79 article-title: Linear mtDNA fragments and unusual mtDNA rearrangements associated with pathological deficiency of MGME1 exonuclease publication-title: Hum. Mol. Genet. doi: 10.1093/hmg/ddu336 – volume: 124 start-page: 209 year: 2012 ident: ref_81 article-title: Clonally expanded mitochondrial DNA deletions within the choroid plexus in multiple sclerosis publication-title: Acta Neuropathol. doi: 10.1007/s00401-012-1001-9 – volume: 27 start-page: 223 year: 2016 ident: ref_76 article-title: Microhomology-mediated end joining is the principal mediator of double-strand break repair during mitochondrial DNA lesions publication-title: Mol. Biol. Cell doi: 10.1091/mbc.e15-05-0260 – volume: 276 start-page: 5768 year: 2009 ident: ref_1 article-title: Is there more to aging than mitochondrial DNA and reactive oxygen species? publication-title: FEBS J. doi: 10.1111/j.1742-4658.2009.07269.x – ident: ref_13 doi: 10.1371/journal.pgen.1003974 – volume: 1777 start-page: 853 year: 2008 ident: ref_11 article-title: Mitigation of NADH: Ubiquinone oxidoreductase deficiency by chronic Trolox treatment publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbabio.2008.03.028 – volume: 102 start-page: 18769 year: 2005 ident: ref_59 article-title: The mitochondrial theory of aging and its relationship to reactive oxygen species damage and somatic mtDNA mutations publication-title: Proc. Natl Acad. Sci. USA doi: 10.1073/pnas.0509776102 – volume: 8 start-page: 341 year: 2007 ident: ref_32 article-title: Assessment of chelatable mitochondrial Iron by using mitochondrion-selective fluorescent iron indicators with different iron-binding affinities publication-title: Chem. Bio. Chem. doi: 10.1002/cbic.200600311 – volume: 5 start-page: 279 year: 2006 ident: ref_54 article-title: Does premature aging of the mtDNA mutator mouse prove that mtDNA mutations are involved in natural aging? publication-title: Aging Cell doi: 10.1111/j.1474-9726.2006.00209.x – volume: 2 start-page: 318 year: 1992 ident: ref_6 article-title: Mosaicism for a specific somatic mitochondrial DNA mutation in adult human brain publication-title: Nat. Genet. doi: 10.1038/ng1292-318 – ident: ref_45 doi: 10.1371/journal.pgen.1003794 – volume: 61 start-page: 1175 year: 1992 ident: ref_16 article-title: Diseases of the mitochondrial DNA publication-title: Annu. Rev. Biochem. doi: 10.1146/annurev.bi.61.070192.005523 – volume: 48 start-page: 766 year: 2000 ident: ref_92 article-title: Mitochondrial complex I deficiency in the epileptic focus of patients with temporal lobe epilepsy publication-title: Ann. Neurol. doi: 10.1002/1531-8249(200011)48:5<766::AID-ANA10>3.0.CO;2-M – volume: 33 start-page: 89 year: 2017 ident: ref_48 article-title: Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases publication-title: Ageing Res. Rev. doi: 10.1016/j.arr.2016.04.006 – volume: 61 start-page: 325 year: 2017 ident: ref_2 article-title: Origins of mtDNA mutations in ageing publication-title: Essays Biochem. doi: 10.1042/EBC20160090 – volume: 27 start-page: 2434 year: 1999 ident: ref_69 article-title: Cell-by-cell scanning of whole mitochondrial genomes in aged human heart reveals a significant fraction of myocytes with clonally expanded deletions publication-title: Nucleic Acids Res. doi: 10.1093/nar/27.11.2434 – volume: 273 start-page: 23690 year: 1998 ident: ref_57 article-title: The role of 3′-5′ exonucleolytic proofreading and mismatch repair in yeast mitochondrial DNA error avoidance publication-title: J. Biol. Chem. doi: 10.1074/jbc.273.37.23690 – volume: 43 start-page: 806 year: 2011 ident: ref_71 article-title: Mitochondrial aging is accelerated by anti-retroviral therapy through the clonal expansion of mtDNA mutations publication-title: Nat. Genet. doi: 10.1038/ng.863 – volume: 400 start-page: 99 year: 1998 ident: ref_41 article-title: Mutagenicity and repair of oxidative DNA damage: Insights from studies using defined lesions publication-title: Mutat. Res. doi: 10.1016/S0027-5107(98)00066-9 – volume: 33 start-page: 18270 year: 2013 ident: ref_25 article-title: Microglial CD33-related Siglec-E inhibits neurotoxicity by preventing the phagocytosis-associated oxidative burst publication-title: J. Neurosci. doi: 10.1523/JNEUROSCI.2211-13.2013 – ident: ref_58 doi: 10.1371/journal.pone.0011468 – volume: 21 start-page: 667 year: 2015 ident: ref_20 article-title: Mosaic deficiency in mitochondrial oxidative metabolism promotes cardiac arrhythmia during aging publication-title: Cell Metab. doi: 10.1016/j.cmet.2015.04.005 – volume: 9 start-page: 536 year: 2010 ident: ref_61 article-title: Age-dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria publication-title: Aging Cell doi: 10.1111/j.1474-9726.2010.00581.x – volume: 51 start-page: 692 year: 2006 ident: ref_37 article-title: Proteins associated with mitochondrial DNA protect it against the action of X-rays and hydrogen peroxide publication-title: Biofizika – volume: 26 start-page: 340 year: 2010 ident: ref_75 article-title: Repeats, longevity and the sources of mtDNA deletions: Evidence from ‘deletional spectra’ publication-title: Trends Genet. doi: 10.1016/j.tig.2010.05.006 – volume: 22 start-page: 266 year: 2016 ident: ref_83 article-title: The Parkinson disease mitochondrial hypothesis: Where are we at? publication-title: Neuroscientist doi: 10.1177/1073858415574600 – volume: 271 start-page: 21177 year: 1996 ident: ref_39 article-title: Oxidative damage to DNA constituents by iron-mediated Fenton reactions. The deoxyguanosine family publication-title: J. Biol. Chem. doi: 10.1074/jbc.271.35.21177 – volume: 40 start-page: 392 year: 2008 ident: ref_60 article-title: DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice publication-title: Nat. Genet. doi: 10.1038/ng.95 – volume: 17 start-page: 843 year: 1996 ident: ref_66 article-title: Cytochrome c oxidase defects of the human substantia nigra in normal aging publication-title: Neurobiol. Aging doi: 10.1016/S0197-4580(96)00168-6 – volume: 38 start-page: 518 year: 2006 ident: ref_10 article-title: Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons publication-title: Nat. Genet. doi: 10.1038/ng1778 – volume: 71 start-page: 60 year: 2006 ident: ref_42 article-title: Hydrogen peroxide produced inside mitochondria takes part in cell-to-cell transmission of apoptotic signal publication-title: Biochemistry – volume: 9 start-page: 1447 year: 2017 ident: ref_35 article-title: Subcellular compartmentalisation of copper, iron, manganese, and zinc in the Parkinson’s disease brain publication-title: Metallomics doi: 10.1039/C7MT00244K – volume: 12 start-page: 484 year: 2002 ident: ref_70 article-title: Ageing muscle: Clonal expansions of mitochondrial DNA point mutations and deletions cause focal impairment of mitochondrial function publication-title: Neuromuscul. Disord. doi: 10.1016/S0960-8966(01)00332-7 – volume: 120 start-page: 419 year: 2012 ident: ref_86 article-title: Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer’s disease publication-title: J. Neurochem. doi: 10.1111/j.1471-4159.2011.07581.x – reference: 1303287 - Nat Genet. 1992 Dec;2(4):318-23 – reference: 17005554 - J Biol Chem. 2006 Nov 24;281(47):36236-40 – reference: 26182419 - Neuron. 2015 Jul 15;87(2):371-81 – reference: 11809722 - Hum Mol Genet. 2002 Jan 15;11(2):133-45 – reference: 15164064 - Nature. 2004 May 27;429(6990):417-23 – reference: 25409153 - Nature. 2015 Jan 29;517(7536):635-9 – reference: 16604074 - Nat Genet. 2006 May;38(5):515-7 – reference: 18435906 - Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):853-9 – reference: 22718549 - Ann Neurol. 2012 Jun;71(6):850-4 – reference: 28453550 - PLoS One. 2017 Apr 28;12 (4):e0176795 – reference: 2554297 - Proc Natl Acad Sci U S A. 1989 Oct;86(20):7952-6 – reference: 19061483 - Biochem J. 2009 Jan 1;417(1):1-13 – reference: 16909848 - Biofizika. 2006 Jul-Aug;51(4):692-7 – reference: 25299268 - Sci Rep. 2014 Oct 09;4:6569 – reference: 1303288 - Nat Genet. 1992 Dec;2(4):324-9 – reference: 24621297 - Aging Cell. 2014 Aug;13(4):765-8 – reference: 24986917 - Hum Mol Genet. 2014 Dec 1;23(23):6147-62 – reference: 749453 - Acta Biol Med Ger. 1978;37(8):1167-76 – reference: 17956319 - Biochem Soc Trans. 2007 Nov;35(Pt 5):1228-31 – reference: 28209927 - Aging (Albany NY). 2017 Feb 15;9(2):315-339 – reference: 16365283 - Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18769-70 – reference: 16457620 - Biochemistry (Mosc). 2006 Jan;71(1):60-7 – reference: 2541614 - Am J Pathol. 1989 May;134(5):1167-73 – reference: 11336636 - Biochem J. 2001 May 15;356(Pt 1):61-9 – reference: 29281123 - FEBS Lett. 2018 Mar;592(5):728-742 – reference: 11943860 - Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5521-6 – reference: 26609070 - Mol Biol Cell. 2016 Jan 15;27(2):223-35 – reference: 16604072 - Nat Genet. 2006 May;38(5):518-20 – reference: 17219451 - Chembiochem. 2007 Feb 12;8(3):341-52 – reference: 28094012 - Cell Metab. 2017 Jan 10;25(1):57-71 – reference: 21706004 - Nat Genet. 2011 Jun 26;43(8):806-10 – reference: 27874000 - Nat Commun. 2016 Nov 22;7:13548 – reference: 16020738 - Science. 2005 Jul 15;309(5733):481-4 – reference: 17090418 - Free Radic Res. 2006 Dec;40(12):1284-94 – reference: 12031622 - Neuromuscul Disord. 2002 Jun;12(5):484-93 – reference: 27315116 - Ann Neurol. 2016 Aug;80(2):301-6 – reference: 11156948 - FASEB J. 2001 Feb;15(2):322-32 – reference: 15181170 - Nucleic Acids Res. 2004 Jun 04;32(10):3053-64 – reference: 11978482 - Free Radic Biol Med. 2002 May 1;32(9):804-12 – reference: 15703189 - Hum Mol Genet. 2005 Apr 1;14(7):893-902 – reference: 22688405 - Acta Neuropathol. 2012 Aug;124(2):209-20 – reference: 11079540 - Ann Neurol. 2000 Nov;48(5):766-73 – reference: 19309719 - Hepatology. 2009 May;49(5):1655-63 – reference: 25149213 - Prog Mol Biol Transl Sci. 2014;127:29-62 – reference: 25991500 - Biopolymers. 2015 Sep;103(9):491-508 – reference: 9726974 - J Biol Chem. 1998 Sep 11;273(37):23690-7 – reference: 20456298 - Aging Cell. 2010 Aug;9(4):536-44 – reference: 20628647 - PLoS One. 2010 Jul 07;5(7):e11468 – reference: 24596558 - Front Pharmacol. 2014 Feb 17;5:19 – reference: 28698307 - Essays Biochem. 2017 Jul 11;61(3):325-337 – reference: 21368114 - Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4135-40 – reference: 1965203 - J Neurol Sci. 1990 Dec;100(1-2):14-21 – reference: 28944802 - Metallomics. 2017 Oct 18;9(10 ):1447-1455 – reference: 29257976 - Neurobiol Aging. 2018 Mar;63:120-127 – reference: 22225879 - Cell Metab. 2012 Jan 4;15(1):100-9 – reference: 1849843 - FEBS Lett. 1991 Apr 9;281(1-2):9-19 – reference: 1321035 - EMBO J. 1992 Jul;11(7):2717-26 – reference: 23965628 - Nature. 2013 Sep 19;501(7467):412-5 – reference: 10325435 - Nucleic Acids Res. 1999 Jun 1;27(11):2434-41 – reference: 19036942 - Am J Physiol Cell Physiol. 2009 Feb;296(2):C355-62 – reference: 21826691 - Bioessays. 2011 Oct;33(10):742-8 – reference: 25955204 - Cell Metab. 2015 May 5;21(5):667-77 – reference: 20591530 - Trends Genet. 2010 Aug;26(8):340-3 – reference: 17725985 - Hum Mol Genet. 2007 Nov 15;16(22):2729-39 – reference: 19095717 - Hum Mol Genet. 2009 Mar 15;18(6):1028-36 – reference: 9363794 - Neurobiol Aging. 1996 Nov-Dec;17(6):843-8 – reference: 17005553 - J Biol Chem. 2006 Nov 24;281(47):36241-8 – reference: 11141179 - J Exp Bot. 2000 Dec;51(353):2053-66 – reference: 25761946 - Neuroscientist. 2016 Jun;22(3):266-77 – reference: 18305478 - Nat Genet. 2008 Mar;40(3):275-9 – reference: 11381261 - Nat Genet. 2001 Jun;28(2):147-50 – reference: 26993140 - Acta Neuropathol. 2016 Aug;132(2):277-88 – reference: 24516391 - PLoS Genet. 2014 Feb 06;10(2):e1003974 – reference: 22077634 - J Neurochem. 2012 Feb;120(3):419-29 – reference: 14597761 - J Clin Invest. 2003 Nov;112(9):1351-60 – reference: 18948172 - Biochim Biophys Acta. 2009 Jul;1790(7):629-36 – reference: 24086148 - PLoS Genet. 2013;9(9):e1003794 – reference: 1497308 - Annu Rev Biochem. 1992;61:1175-212 – reference: 20937894 - Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18670-5 – reference: 19796285 - FEBS J. 2009 Oct;276(20):5768-87 – reference: 8702888 - J Biol Chem. 1996 Aug 30;271(35):21177-86 – reference: 9685598 - Mutat Res. 1998 May 25;400(1-2):99-115 – reference: 25176146 - Cell Metab. 2014 Oct 7;20(4):662-9 – reference: 20211146 - Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1163-70 – reference: 24987008 - Physiol Rev. 2014 Jul;94(3):909-50 – reference: 18311139 - Nat Genet. 2008 Apr;40(4):392-4 – reference: 14625276 - J Biol Chem. 2004 Feb 6;279(6):4127-35 – reference: 27143693 - Ageing Res Rev. 2017 Jan;33:89-104 – reference: 16392116 - Ann Neurol. 2006 Mar;59(3):478-89 – reference: 28441057 - Annu Rev Biochem. 2017 Jun 20;86:715-748 – reference: 21446022 - Ann Neurol. 2011 Mar;69(3):481-92 – reference: 19244310 - Nucleic Acids Res. 2009 Apr;37(7):2327-35 – reference: 16842501 - Aging Cell. 2006 Jun;5(3):279-82 – reference: 11829750 - Biochem J. 2002 Feb 15;362(Pt 1):137-47 – reference: 24227736 - J Neurosci. 2013 Nov 13;33(46):18270-6 – reference: 21406249 - Mitochondrion. 2012 Mar;12(2):173-9 |
| SSID | ssj0000402005 |
| Score | 2.3207185 |
| SecondaryResourceType | review_article |
| Snippet | Recent deep sequencing data has provided compelling evidence that the spectrum of somatic point mutations in mitochondrial DNA (mtDNA) in aging tissues lacks G... |
| SourceID | pubmedcentral proquest pubmed crossref |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 175 |
| SubjectTerms | Aging Deoxyribonucleic acid DNA DNA sequencing DNA-directed DNA polymerase Hydrogen peroxide Mitochondrial DNA Mutation Oxidative stress Reactive oxygen species Review Transversion |
| SummonAdditionalLinks | – databaseName: ProQuest Central dbid: BENPR link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3dS9xAEB_0pOCLtFo1VssK9qmE5vYjmzwUOauigtdyVvAtJLsbPThyp0bQ_74z-fKs6Gt2YMPs7nzszvx-AHtKCisjQwTEQvtSp8JHPy_8PA20RY9ts6pJ7HwYnlzKsyt1tQDDtheGyipbm1gZajs1dEeOSTpmIopLpfdntz6xRtHrakuhkTbUCvZnBTG2CEtoklXQg6WDo-GfUXfrElC6FKi6Al5gvv_jmkxKjN_7VGo475teBZz_103OOaLjj7DSRJBsUC_5J1hwxSp8qDkln9ZgdHrPcO3vHLsoxxOUK57YaDpxDKNT9vtxbCukb3ZR9YiwccHO8UyjDSwsbUV2OBz4hw0xbskGRGG0_xkuj4_-_jrxG-IE38g-L_2Mh0Iawa20Kk-ti6M04LnjIjax03kWC6OUI3ZOo1EgjHMRyiATmTBGcpmKdegV08JtAtPUCCu4sy4MZRYQlKGhl9VIxUY4pz343qosMQ2qOJFbTBLMLkjBybyCPfjWSc9qNI035LZb7SfNmbpPnneAB7vdMJ4GeuJICzd9IJkKHkiK0IONerG6iTj18EZB5IF-sYydACFtvxwpxjcV4rbCLFX19db7v_UFlnH-qmOR97ehV949uB0MWcrsa7MP_wGu_-v1 priority: 102 providerName: ProQuest |
| Title | Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging? |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/29561808 https://www.proquest.com/docview/2040952457 https://www.proquest.com/docview/2017055436 https://pubmed.ncbi.nlm.nih.gov/PMC5924517 |
| Volume | 9 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3dS-NAEB_8QPBF9D60d56s4D0dOdP9yCYPh9QvVLB3VAu-hWR3o4WSao1g_3tnNmmxegf3GHbIwszszgw78_sB7CkprIwNERALHUidiQDjvAiKLNQWI7bN_ZDYZTc668uLG3WzAFO20UaBj38t7YhPqj8e_nx-mBzggf9FFSeW7Pu3dCsk6I0YChdh2b8UURNfk-j7O5nKJN_PyNGnA4meWnfBv_vBfHx6l3S-7Z18FYxO12GtySJZpzb7Biy48gOs1LySk4_QO39kaP-xY1fVYIhy5YT1RkPHMENlv58H1qN9sys_J8IGJbvEc42qKC25IzvudoLjhhy3Yh2iMTr4BP3Tk-ujs6AhTwiMbPMqyHkkpBHcSquKzLokzkJeOC4Skzhd5IkwSjli6DQaBaKkEJEMc5ELYySXmfgMS-WodFvANA3DCu6siyKZhwRnaOh1NVaJEc7pFvyYqiw1DbI4EVwMU6wwSMHpawW34PtM-r5G1PiH3PZU--nULVKOa4niUuGmu7NlPBH0zJGVbvREMh4iSIqoBZu1sWYbcZrjjcO4BXrOjDMBQtueXykHdx51W2Glqtr6y3_s-xVW8cOPLvL2NixV4yf3DXOXKt-B5cOT7p_ejnfPF-dZ7bc |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEB6VVAguiDeGAotET8jC2YfXPlRVIK0S2gSUtlJvxt5dt5EipzSuIH-O38aM7ZgUBLdevSPbmp2d2dmd-T6At0oKKyNDBMRC-1Knwsc4L_w8DbTFiG2zqklsNA4HJ_LTqTrdgJ-rXhgqq1z5xMpR27mhM3JM0jETUVwqvXvxzSfWKLpdXVFopA21gt2pIMaaxo4Dt_yOKdxiZ9jH-d7mfH_v-OPAb1gGfCO7vPQzHgppBLfSqjy1Lo7SgOeOi9jETudZLIxSjqgsjUaBMM5FKINMZMIYyWUq8L23YFPSAUoHNj_sjb9M2lOegNKzQNUV90LEwfszcmExPu9SaeN6LPxrg_tnneZa4Nu_D_eaHSvr1Sb2ADZc8RBu1xyWy0cwGS4Y2tqlY0fldIZyxZJN5jPHcDfMPv-Y2gpZnB1VPSlsWrAR-hD0uYUl02f9cc_vN0S8JesRZdLuYzi5ERU-gU4xL9wzYJoabwV31oWhzAKCTjR0kxup2AjntAfvVipLTINiTmQaswSzGVJwsq5gD7Zb6YsaveMfclsr7SfNGl4kvy3OgzftMK4-ulJJCze_IpkKjkiK0IOn9WS1H-LUMxwFkQf62jS2AoTsfX2kmJ5XCN8Ks2LV1c___1uv4c7geHSYHA7HBy_gLv5L1S3Ju1vQKS-v3EvcLpXZq8YmGXy96WXwCxKrKW0 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEB6VViAuiDeGAotET8jC2YfXPlRVII0aSkOVUqk3195d00iR0zauIH-RX8WMX6QguPXqHdmr2Xl6Z-YDeKuksDIyBEAstC91Knz088LP00Bb9Ng2q5rEDsbh3rH8dKJO1uBn2wtDZZWtTawMtZ0b-keOSTpmIopLTODzpizicDDcOb_wCUGKblpbOI20gVmw29W4sabJY98tv2M6t9geDfDstzgf7n79uOc3iAO-kT1e-hkPhTSCW2lVnloXR2nAc8dFbGKn8ywWRilHsJZGI0EY5yKUQSYyYYzkMhX43luwodHrYyK48WF3fDjp_vgElKoFqq6-FyIO3n8jcxbj8x6VOa76xb-C3T9rNlec4PA-3GuiV9avxe0BrLniIdyu8SyXj2AyWjCUu0vHjsrpDOmKJZvMZ45hZMy-_Jjaaso4O6r6U9i0YAdoT9D-FpbUgA3GfX_QgPKWrE_wSTuP4fhGWPgE1ot54Z4B09SEK7izLgxlFtAYRUO3upGKjXBOe_CuZVlimonmBKwxSzCzIQYnqwz2YKujPq8nefyDbrPlftLo8yL5LX0evOmWURPpeiUt3PyKaKrRRFKEHjytD6v7EKf-4SiIPNDXjrEjoCnf11eK6Vk17Vthhqx6-vn_t_Ua7qA6JJ9H4_0XcBe3UjVO8t4mrJeXV-4lRk5l9qoRSQanN60FvwDZJy2x |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Is+There+Still+Any+Role+for+Oxidative+Stress+in+Mitochondrial+DNA-Dependent+Aging%3F&rft.jtitle=Genes&rft.au=Zsurka%2C+G%C3%A1bor&rft.au=Peeva%2C+Viktoriya&rft.au=Kotlyar%2C+Alexander&rft.au=Kunz%2C+Wolfram+S&rft.date=2018-03-21&rft.issn=2073-4425&rft.eissn=2073-4425&rft.volume=9&rft.issue=4&rft_id=info:doi/10.3390%2Fgenes9040175&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2073-4425&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2073-4425&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2073-4425&client=summon |