Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0049215
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dc.titleEffects of Hydrogen Peroxide on Wound Healing in Mice in Relation to Oxidative Damage
dc.contributor.authorLoo, A.E.K.
dc.contributor.authorWong, Y.T.
dc.contributor.authorHo, R.
dc.contributor.authorWasser, M.
dc.contributor.authorDu, T.
dc.contributor.authorNg, W.T.
dc.contributor.authorHalliwell, B.
dc.date.accessioned2014-10-27T08:27:03Z
dc.date.available2014-10-27T08:27:03Z
dc.date.issued2012-11-13
dc.identifier.citationLoo, A.E.K., Wong, Y.T., Ho, R., Wasser, M., Du, T., Ng, W.T., Halliwell, B. (2012-11-13). Effects of Hydrogen Peroxide on Wound Healing in Mice in Relation to Oxidative Damage. PLoS ONE 7 (11) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0049215
dc.identifier.issn19326203
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/100546
dc.description.abstractIt has been established that low concentrations of hydrogen peroxide (H2O2) are produced in wounds and is required for optimal healing. Yet at the same time, there is evidence that excessive oxidative damage is correlated with poor-healing wounds. In this paper, we seek to determine whether topical application of H2O2 can modulate wound healing and if its effects are related to oxidative damage. Using a C57BL/6 mice excision wound model, H2O2 was found to enhance angiogenesis and wound closure at 10 mM but retarded wound closure at 166 mM. The delay in closure was also associated with decreased connective tissue formation, increased MMP-8 and persistent neutrophil infiltration. Wounding was found to increase oxidative lipid damage, as measured by F2-isoprostanes, and nitrative protein damage, as measured by 3-nitrotyrosine. However H2O2 treatment did not significantly increase oxidative and nitrative damage even at concentrations that delay wound healing. Hence the detrimental effects of H2O2 may not involve oxidative damage to the target molecules studied. © 2012 Loo et al.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1371/journal.pone.0049215
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1371/journal.pone.0049215
dc.description.sourcetitlePLoS ONE
dc.description.volume7
dc.description.issue11
dc.description.page-
dc.identifier.isiut000311234600030
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