Editing Epigenetics (section)

===DNA damage===
DNA damage can also cause epigenetic changes.<ref>{{cite journal | vauthors = Kovalchuk O, Baulch JE | title = Epigenetic changes and nontargeted radiation effects--is there a link? | journal = Environmental and Molecular Mutagenesis | volume = 49 | issue = 1 | pages = 16–25 | date = January 2008 | pmid = 18172877 | doi = 10.1002/em.20361 | bibcode = 2008EnvMM..49...16K | s2cid = 38705208 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Ilnytskyy Y, Kovalchuk O | title = Non-targeted radiation effects-an epigenetic connection | journal = Mutation Research | volume = 714 | issue = 1–2 | pages = 113–25 | date = September 2011 | pmid = 21784089 | doi = 10.1016/j.mrfmmm.2011.06.014 | bibcode = 2011MRFMM.714..113I }}</ref><ref>{{cite journal | vauthors = Friedl AA, Mazurek B, Seiler DM | title = Radiation-induced alterations in histone modification patterns and their potential impact on short-term radiation effects | journal = Frontiers in Oncology | volume = 2 | pages = 117 | year = 2012 | pmid = 23050241 | pmc = 3445916 | doi = 10.3389/fonc.2012.00117 | doi-access = free }}</ref> DNA damage is very frequent, occurring on average about 60,000 times a day per cell of the human body (see [[DNA damage (naturally occurring)]]). These damages are largely repaired, however, epigenetic changes can still remain at the site of DNA repair.<ref name="Cuozzo" /> In particular, a double strand break in DNA can initiate unprogrammed epigenetic gene silencing both by causing DNA methylation as well as by promoting silencing types of histone modifications (chromatin remodeling - see next section).<ref>{{cite journal | vauthors = O'Hagan HM, Mohammad HP, Baylin SB | title = Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island | journal = PLOS Genetics | volume = 4 | issue = 8 | pages = e1000155 | date = August 2008 | pmid = 18704159 | pmc = 2491723 | doi = 10.1371/journal.pgen.1000155 | veditors = Lee JT | doi-access = free }}</ref> In addition, the enzyme [[Poly ADP ribose polymerase|Parp1 (poly(ADP)-ribose polymerase)]] and its product poly(ADP)-ribose (PAR) accumulate at sites of DNA damage as part of the repair process.<ref>{{cite journal | vauthors = Malanga M, Althaus FR | title = The role of poly(ADP-ribose) in the DNA damage signaling network | journal = Biochemistry and Cell Biology | volume = 83 | issue = 3 | pages = 354–64 | date = June 2005 | pmid = 15959561 | doi = 10.1139/o05-038 | url = https://www.zora.uzh.ch/id/eprint/5838/1/RPViewDoc.pdf }}</ref> This accumulation, in turn, directs recruitment and activation of the chromatin remodeling protein, ALC1, that can cause [[nucleosome]] remodeling.<ref>{{cite journal | vauthors = Gottschalk AJ, Timinszky G, Kong SE, Jin J, Cai Y, Swanson SK, Washburn MP, Florens L, Ladurner AG, Conaway JW, Conaway RC | title = Poly(ADP-ribosyl)ation directs recruitment and activation of an ATP-dependent chromatin remodeler | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 106 | issue = 33 | pages = 13770–4 | date = August 2009 | pmid = 19666485 | pmc = 2722505 | doi = 10.1073/pnas.0906920106 | bibcode = 2009PNAS..10613770G | doi-access = free }}</ref> Nucleosome remodeling has been found to cause, for instance, epigenetic silencing of DNA repair gene MLH1.<ref name="isbn0-87969-490-4"/><ref>{{cite journal | vauthors = Lin JC, Jeong S, Liang G, Takai D, Fatemi M, Tsai YC, Egger G, Gal-Yam EN, Jones PA | title = Role of nucleosomal occupancy in the epigenetic silencing of the MLH1 CpG island | journal = Cancer Cell | volume = 12 | issue = 5 | pages = 432–44 | date = November 2007 | pmid = 17996647 | pmc = 4657456 | doi = 10.1016/j.ccr.2007.10.014 }}</ref> DNA damaging chemicals, such as [[benzene]], [[hydroquinone]], [[styrene]], [[carbon tetrachloride]] and [[trichloroethylene]], cause considerable hypomethylation of DNA, some through the activation of oxidative stress pathways.<ref>{{cite journal | vauthors = Tabish AM, Poels K, Hoet P, Godderis L | title = Epigenetic factors in cancer risk: effect of chemical carcinogens on global DNA methylation pattern in human TK6 cells | journal = PLOS ONE | volume = 7 | issue = 4 | pages = e34674 | year = 2012 | pmid = 22509344 | pmc = 3324488 | doi = 10.1371/journal.pone.0034674 | veditors = Chiariotti L | bibcode = 2012PLoSO...734674T | doi-access = free }}</ref>

Foods are known to alter the epigenetics of rats on different diets.<ref>{{cite journal | vauthors = Burdge GC, Hoile SP, Uller T, Thomas NA, Gluckman PD, Hanson MA, [[Karen A. Lillycrop|Lillycrop KA]] | title = Progressive, transgenerational changes in offspring phenotype and epigenotype following nutritional transition | journal = PLOS ONE | volume = 6 | issue = 11 | pages = e28282 | year = 2011 | pmid = 22140567 | pmc = 3227644 | doi = 10.1371/journal.pone.0028282 | veditors = Imhof A | bibcode = 2011PLoSO...628282B | doi-access = free }}</ref> Some food components epigenetically increase the levels of DNA repair enzymes such as [[O-6-methylguanine-DNA methyltransferase|MGMT]] and [[MLH1]]<ref>{{cite journal | vauthors = Fang M, Chen D, Yang CS | title = Dietary polyphenols may affect DNA methylation | journal = The Journal of Nutrition | volume = 137 | issue = 1 Suppl | pages = 223S–228S | date = January 2007 | pmid = 17182830 | doi = 10.1093/jn/137.1.223S | doi-access = free }}</ref> and [[p53]].<ref>{{cite journal | vauthors = Olaharski AJ, Rine J, Marshall BL, Babiarz J, Zhang L, Verdin E, Smith MT | title = The flavoring agent dihydrocoumarin reverses epigenetic silencing and inhibits sirtuin deacetylases | journal = PLOS Genetics | volume = 1 | issue = 6 | pages = e77 | date = December 2005 | pmid = 16362078 | pmc = 1315280 | doi = 10.1371/journal.pgen.0010077 | doi-access = free }}</ref> Other food components can reduce DNA damage, such as soy [[isoflavones]]. In one study, markers for oxidative stress, such as modified nucleotides that can result from DNA damage, were decreased by a 3-week diet supplemented with soy.<ref>{{cite journal | vauthors = Djuric Z, Chen G, Doerge DR, Heilbrun LK, Kucuk O | title = Effect of soy isoflavone supplementation on markers of oxidative stress in men and women | journal = Cancer Letters | volume = 172 | issue = 1 | pages = 1–6 | date = October 2001 | pmid = 11595123 | doi = 10.1016/S0304-3835(01)00627-9 }}</ref> A decrease in oxidative DNA damage was also observed 2 h after consumption of [[anthocyanin]]-rich [[bilberry]] (''[[Vaccinium myrtillus|Vaccinium myrtillius]]'' L.) [[pomace]] extract.<ref>{{cite journal | vauthors = Kropat C, Mueller D, Boettler U, Zimmermann K, Heiss EH, Dirsch VM, Rogoll D, Melcher R, Richling E, Marko D | title = Modulation of Nrf2-dependent gene transcription by bilberry anthocyanins in vivo | journal = Molecular Nutrition & Food Research | volume = 57 | issue = 3 | pages = 545–50 | date = March 2013 | pmid = 23349102 | doi = 10.1002/mnfr.201200504 }}</ref>