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Article: Mequindox induced cellular DNA damage via generation of reactive oxygen species

TitleMequindox induced cellular DNA damage via generation of reactive oxygen species
Authors
Issue Date2012
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/gentox
Citation
Mutation Research - Genetic Toxicology And Environmental Mutagenesis, 2012, v. 741 n. 1-2, p. 70-75 How to Cite?
Abstract
Mequindox, a quinoxaline-N-dioxide derivative that possesses antibacterial properties, has been widely used as a feed additive in the stockbreeding industry in China. While recent pharmacological studies have uncovered potential hazardous effects of mequindox, exactly how mequindox induces pathological changes and the cellular responses associated with its consumption remain largely unexplored. In this study, we investigated the cellular responses associated with mequindox treatment. We report here that mequindox inhibits cell proliferation by arresting cells at the G2/M phase of the cell cycle. Interestingly, this mequindox-associated deleterious effect on cell proliferation was observed in human, pig as well as chicken cells, suggesting that mequindox acts on evolutionarily conserved target(s). To further understand the mequindox-host interaction and the mechanism underlying mequindox-induced cell cycle arrest, we measured the cellular content of DNA damage, which is known to perturb cell proliferation and compromise cell survival. Accordingly, using γ-H2AX as a surrogate marker for DNA damage, we found that mequindox treatment induced cellular DNA damage, which paralleled the chemical-induced elevation of reactive oxygen species (ROS) levels. Importantly, expression of the antioxidant enzyme catalase partially alleviated these mequindox-associated effects. Taken together, our results suggest that mequindox cytotoxicity is attributable, in part, to its role as a potent inducer of DNA damage via ROS. © 2011 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/144508
ISSN
2013 Impact Factor: 2.481
2013 SCImago Journal Rankings: 0.833
ISI Accession Number ID
Funding AgencyGrant Number
National Basic Research Program of China (973 Program)2009CB118802
Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme
Program for New Century Excellent Talents in UniversityNCET-08-0643
Guangdong Province Universities and Colleges Special Funds for Talents
Funding Information:

This work was supported by the National Basic Research Program of China (973 Program), no: 2009CB118802; Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (2009); The Program for New Century Excellent Talents in University, no: NCET-08-0643; Guangdong Province Universities and Colleges Special Funds for Talents (2010).

References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorOuyang, Men_HK
dc.contributor.authorJiang, Jen_HK
dc.contributor.authorMu, Pen_HK
dc.contributor.authorWu, Jen_HK
dc.contributor.authorYang, Qen_HK
dc.contributor.authorZhang, Cen_HK
dc.contributor.authorXu, Wen_HK
dc.contributor.authorWang, Len_HK
dc.contributor.authorHuen, MSYen_HK
dc.contributor.authorDeng, Yen_HK
dc.date.accessioned2012-02-03T06:11:39Z-
dc.date.available2012-02-03T06:11:39Z-
dc.date.issued2012en_HK
dc.identifier.citationMutation Research - Genetic Toxicology And Environmental Mutagenesis, 2012, v. 741 n. 1-2, p. 70-75en_HK
dc.identifier.issn1383-5718en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144508-
dc.description.abstractMequindox, a quinoxaline-N-dioxide derivative that possesses antibacterial properties, has been widely used as a feed additive in the stockbreeding industry in China. While recent pharmacological studies have uncovered potential hazardous effects of mequindox, exactly how mequindox induces pathological changes and the cellular responses associated with its consumption remain largely unexplored. In this study, we investigated the cellular responses associated with mequindox treatment. We report here that mequindox inhibits cell proliferation by arresting cells at the G2/M phase of the cell cycle. Interestingly, this mequindox-associated deleterious effect on cell proliferation was observed in human, pig as well as chicken cells, suggesting that mequindox acts on evolutionarily conserved target(s). To further understand the mequindox-host interaction and the mechanism underlying mequindox-induced cell cycle arrest, we measured the cellular content of DNA damage, which is known to perturb cell proliferation and compromise cell survival. Accordingly, using γ-H2AX as a surrogate marker for DNA damage, we found that mequindox treatment induced cellular DNA damage, which paralleled the chemical-induced elevation of reactive oxygen species (ROS) levels. Importantly, expression of the antioxidant enzyme catalase partially alleviated these mequindox-associated effects. Taken together, our results suggest that mequindox cytotoxicity is attributable, in part, to its role as a potent inducer of DNA damage via ROS. © 2011 Elsevier B.V.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/gentoxen_HK
dc.relation.ispartofMutation Research - Genetic Toxicology and Environmental Mutagenesisen_HK
dc.subject.meshAnimal Husbandryen_HK
dc.subject.meshAnti-Bacterial Agents - toxicityen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Survival - drug effectsen_HK
dc.subject.meshDNA Damageen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMutagens - toxicityen_HK
dc.subject.meshQuinoxalines - toxicityen_HK
dc.subject.meshReactive Oxygen Species - metabolismen_HK
dc.titleMequindox induced cellular DNA damage via generation of reactive oxygen speciesen_HK
dc.typeArticleen_HK
dc.identifier.emailHuen, MSY:huen.michael@hku.hken_HK
dc.identifier.authorityHuen, MSY=rp01336en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mrgentox.2011.10.012en_HK
dc.identifier.pmid22094289en_HK
dc.identifier.scopuseid_2-s2.0-83955161129en_HK
dc.identifier.hkuros198264en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-83955161129&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume741en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage70en_HK
dc.identifier.epage75en_HK
dc.identifier.isiWOS:000300746800008-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLiu, J=36739597900en_HK
dc.identifier.scopusauthoridOuyang, M=36606787500en_HK
dc.identifier.scopusauthoridJiang, J=24776301400en_HK
dc.identifier.scopusauthoridMu, P=54786873100en_HK
dc.identifier.scopusauthoridWu, J=36740582300en_HK
dc.identifier.scopusauthoridYang, Q=54787147500en_HK
dc.identifier.scopusauthoridZhang, C=54787189500en_HK
dc.identifier.scopusauthoridXu, W=54787165100en_HK
dc.identifier.scopusauthoridWang, L=54787044200en_HK
dc.identifier.scopusauthoridHuen, MSY=23004751500en_HK
dc.identifier.scopusauthoridDeng, Y=7401531432en_HK
dc.identifier.citeulike10014603-

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