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Article: Recent perspectives on the relations between fecal mutagenicity, genotoxicity, and diet

TitleRecent perspectives on the relations between fecal mutagenicity, genotoxicity, and diet
Authors
KeywordsAmes test
Colon
Comet assay
Diet
Dna
Feces
Human
N-nitroso compounds
Issue Date2011
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/pharmacology
Citation
Frontiers In Pharmacology, 2011, v. MAR How to Cite?
AbstractDNA damage is an essential component of the genesis of colonic cancer. Gut microbial products and food components are thought to be principally responsible for the damage that initiates disease progression. Modified Ames tests and Comet assays have been developed for measuring mutagenicity and genotoxicity. Their relevance to oncogenesis remains to be confirmed, as does the relative importance of different mutagenic and genotoxic compounds present in fecal water and the bacteria involved in their metabolism. Dietary intervention studies provide clues to the likely risks of oncogenesis. High-protein diets lead to increases in N-nitroso compounds in fecal water and greater DNA damage as measured by the Comet assay, for example. Other dietary interventions, such as non-digestible carbohydrates and probiotics, may lead to lower fecal genotoxicity. In order to make recommendations to the general public, we must develop a better understanding of how genotoxic compounds are formed in the colon, how accurate the Ames and Comet assays are, and how diet affects genotoxicity. © 2011 Gratz, Wallace and El-Nezami.
Persistent Identifierhttp://hdl.handle.net/10722/136250
ISSN
2015 Impact Factor: 4.418
2015 SCImago Journal Rankings: 1.845
PubMed Central ID
References

 

DC FieldValueLanguage
dc.contributor.authorGratz, SWen_HK
dc.contributor.authorWallace, RJen_HK
dc.contributor.authorElNezami, HSen_HK
dc.date.accessioned2011-07-27T02:11:41Z-
dc.date.available2011-07-27T02:11:41Z-
dc.date.issued2011en_HK
dc.identifier.citationFrontiers In Pharmacology, 2011, v. MARen_HK
dc.identifier.issn1663-9812en_HK
dc.identifier.urihttp://hdl.handle.net/10722/136250-
dc.description.abstractDNA damage is an essential component of the genesis of colonic cancer. Gut microbial products and food components are thought to be principally responsible for the damage that initiates disease progression. Modified Ames tests and Comet assays have been developed for measuring mutagenicity and genotoxicity. Their relevance to oncogenesis remains to be confirmed, as does the relative importance of different mutagenic and genotoxic compounds present in fecal water and the bacteria involved in their metabolism. Dietary intervention studies provide clues to the likely risks of oncogenesis. High-protein diets lead to increases in N-nitroso compounds in fecal water and greater DNA damage as measured by the Comet assay, for example. Other dietary interventions, such as non-digestible carbohydrates and probiotics, may lead to lower fecal genotoxicity. In order to make recommendations to the general public, we must develop a better understanding of how genotoxic compounds are formed in the colon, how accurate the Ames and Comet assays are, and how diet affects genotoxicity. © 2011 Gratz, Wallace and El-Nezami.en_HK
dc.languageengen_US
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/pharmacologyen_HK
dc.relation.ispartofFrontiers in Pharmacologyen_HK
dc.rightsThis Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAmes testen_HK
dc.subjectColonen_HK
dc.subjectComet assayen_HK
dc.subjectDieten_HK
dc.subjectDnaen_HK
dc.subjectFecesen_HK
dc.subjectHumanen_HK
dc.subjectN-nitroso compoundsen_HK
dc.titleRecent perspectives on the relations between fecal mutagenicity, genotoxicity, and dieten_HK
dc.typeArticleen_HK
dc.identifier.emailElNezami, HS: elnezami@hkucc.hku.hken_HK
dc.identifier.authorityElNezami, HS=rp00694en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fphar.2011.00004en_HK
dc.identifier.pmid21779247-
dc.identifier.pmcidPMC3132665-
dc.identifier.scopuseid_2-s2.0-84865980067en_HK
dc.identifier.hkuros188057en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84865980067&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volumeMARen_HK
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridGratz, SW=55275057800en_HK
dc.identifier.scopusauthoridWallace, RJ=7401496291en_HK
dc.identifier.scopusauthoridElNezami, HS=6603690577en_HK

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