Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/65441
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dc.contributorDepartment of Health Technology and Informaticsen_US
dc.contributorDepartment of Rehabilitation Sciencesen_US
dc.contributorSchool of Nursingen_US
dc.creatorWang, EWen_US
dc.creatorCollins, ARen_US
dc.creatorPang, MYCen_US
dc.creatorSiu, PMen_US
dc.creatorLai, CKYen_US
dc.creatorWoo, Jen_US
dc.creatorBenzie, IFFen_US
dc.date.accessioned2017-05-22T02:08:37Z-
dc.date.available2017-05-22T02:08:37Z-
dc.identifier.issn0267-8357en_US
dc.identifier.urihttp://hdl.handle.net/10397/65441-
dc.language.isoenen_US
dc.publisherOxford University Pressen_US
dc.rights© The Author 2016. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved.en_US
dc.rightsThis is a pre-copyedited, author-produced version of an article accepted for publication in Mutagenesis following peer review. The version of record Erica W. Wang, Andrew R. Collins, Marco Y. C. Pang, Parco P. M. Siu, Claudia K. Y. Lai, Jean Woo, Iris F. F. Benzie, Vitamin D and oxidation-induced DNA damage: is there a connection?, Mutagenesis, Volume 31, Issue 6, November 2016, Pages 655–659 is available online at: https://doi.org/10.1093/mutage/gew033.en_US
dc.titleVitamin D and oxidation-induced DNA damage : is there a connection?en_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage655en_US
dc.identifier.epage659en_US
dc.identifier.volume31en_US
dc.identifier.issue6en_US
dc.identifier.doi10.1093/mutage/gew033en_US
dcterms.abstractOxidation-induced damage to DNA can cause mutations, phenotypic changes and apoptosis. Agents that oppose such damage offer potential therapies for disease prevention. Vitamin D administration reportedly lowered DNA damage in type 2 diabetic mice, and higher DNA damage was reported in mononuclear cells of severely asthmatic patients who were vitamin D deficient. We hypothesised that lower vitamin D status associates with higher oxidation-induced DNA damage. Vitamin D deficiency (plasma 25(OH)D < 50 nmol/l) is highly prevalent worldwide, and association with DNA damage has high potential importance and impact in regard to the future health of vitamin D deficient young adults. In this study, oxidation-induced DNA damage in peripheral lymphocytes of 121 young (18-26 years) adults was measured using the formamidopyrimidine DNA glycosylase (FPG)-assisted comet assay. Plasma 25(OH)D was measured by liquid chromatography with tandem mass spectrometry (LC-MS/MS). Correlational analysis was performed between 25(OH)D and DNA damage. Differences in DNA damage across tertiles of 25(OH)D were explored using analysis of variance. DNA damage in those with 25(OH)D <50 nmol and ?50 nmol/l was compared using the unpaired t-test. Mean (SD) DNA damage (as %DNA in comet tail) and plasma 25(OH)D were, respectively, 18.58 (3.39)% and 44.7 (13.03) nmol/l. Most (82/121; 68%) of the subjects were deficient in vitamin D (25(OH)D <50nmol/l). No significant correlation was seen between 25(OH)D and DNA damage (r = -0.0824; P > 0.05). No significant difference was seen across 25(OH)D tertiles: mean (SD) %DNA in comet tail/25(OH)D nmol/l values in lowest, middle and highest tertiles were, respectively, 18.64 (3.30)/31.6 (4.4), 18.90 (3.98)/42.9 (3.5), 18.19 (2.84)/59.9 (8.5), nor across the binary divide: 18.73 (3.63)% in <50nmol/l group vs. 18.27 (2.84)% in the ?50 nmol/l group. No association between vitamin D and oxidation-induced DNA damage was observed, but vitamin D deficiency was highly prevalent in the young adults studied, and we cannot rule out an ameliorative effect of correction of vitamin D deficiency on DNA damage.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationMutagenesis, Nov. 2016, v. 31, no. 6, p. 655-659en_US
dcterms.isPartOfMutagenesisen_US
dcterms.issued2016-11-
dc.identifier.isiWOS:000388015700005-
dc.identifier.scopus2-s2.0-84994476628-
dc.identifier.ros2016001900-
dc.identifier.eissn1464-3804en_US
dc.identifier.rosgroupid2016001864-
dc.description.ros2016-2017 > Academic research: refereed > Publication in refereed journalen_US
dc.description.validate201804_a bcmaen_US
dc.description.oaAccepted Manuscripten_US
dc.identifier.FolderNumbera0821-n03-
dc.identifier.SubFormID1836-
dc.description.fundingSourceRGCen_US
dc.description.fundingTextPolyU 5601/13Men_US
dc.description.pubStatusPublisheden_US
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