Editing Mitochondrial DNA (section)

=== Susceptibility ===
The concept that mtDNA is particularly susceptible to [[reactive oxygen species]] generated by the [[respiratory chain]] due to its proximity remains controversial.<ref name="pmid19796285">{{Cite journal |vauthors=Alexeyev MF |date=October 2009 |title=Is there more to aging than mitochondrial DNA and reactive oxygen species? |journal=The FEBS Journal |volume=276 |issue=20 |pages=5768–5787 |doi=10.1111/j.1742-4658.2009.07269.x |pmc=3097520 |pmid=19796285}}</ref> mtDNA does not accumulate any more oxidative base damage than nuclear DNA.<ref>{{Cite journal |vauthors=Anson RM, Hudson E, Bohr VA |date=February 2000 |title=Mitochondrial endogenous oxidative damage has been overestimated |journal=FASEB Journal |volume=14 |issue=2 |pages=355–360 |doi=10.1096/fasebj.14.2.355 |pmid=10657991 |s2cid=19771110 |doi-access=free}}</ref> It has been reported that at least some types of oxidative DNA damage are repaired more efficiently in mitochondria than they are in the nucleus.<ref>{{Cite journal |vauthors=Thorslund T, Sunesen M, Bohr VA, Stevnsner T |date=April 2002 |title=Repair of 8-oxoG is slower in endogenous nuclear genes than in mitochondrial DNA and is without strand bias |url=https://zenodo.org/record/1260266 |url-status=live |journal=DNA Repair |volume=1 |issue=4 |pages=261–273 |doi=10.1016/S1568-7864(02)00003-4 |pmid=12509245 |archive-url=https://web.archive.org/web/20191231090007/https://zenodo.org/record/1260266 |archive-date=31 December 2019 |access-date=30 June 2019}}</ref> mtDNA is packaged with proteins which appear to be as protective as proteins of the nuclear chromatin.<ref>{{Cite journal |vauthors=Guliaeva NA, Kuznetsova EA, Gaziev AI |year=2006 |title=[Proteins associated with mitochondrial DNA protect it against the action of X-rays and hydrogen peroxide] |trans-title=Proteins associated with mitochondrial DNA protect it against the action of X-rays and hydrogen peroxide |journal=Biofizika |language=ru |volume=51 |issue=4 |pages=692–697 |pmid=16909848}}</ref> Moreover, mitochondria evolved a unique mechanism which maintains mtDNA integrity through degradation of excessively damaged genomes followed by replication of intact/repaired mtDNA.  This mechanism is not present in the nucleus and is enabled by multiple copies of mtDNA present in mitochondria.<ref>{{Cite journal |vauthors=Alexeyev M, Shokolenko I, Wilson G, LeDoux S |date=May 2013 |title=The maintenance of mitochondrial DNA integrity--critical analysis and update |journal=Cold Spring Harbor Perspectives in Biology |volume=5 |issue=5 |pages=a012641 |doi=10.1101/cshperspect.a012641 |pmc=3632056 |pmid=23637283}}</ref> The outcome of mutation in mtDNA may be an alteration in the coding instructions for some proteins,<ref>{{Cite book |title=Encyclopedia of Earth |vauthors=Hogan CM |publisher=National Council for Science and the Environment |year=2010 |veditors=Monosson E, Cleveland CJ |location=Washington DC |chapter=Mutation |access-date=18 April 2011 |chapter-url=http://www.eoearth.org/article/Mutation?topic=49496 |archive-url=https://web.archive.org/web/20110430051516/http://www.eoearth.org/article/Mutation?topic=49496 |archive-date=30 April 2011 |url-status=live}}</ref> which may have an effect on organism metabolism and/or fitness.