File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Vitamin D and oxidation-induced DNA damage: Is there a connection?

TitleVitamin D and oxidation-induced DNA damage: Is there a connection?
Authors
Issue Date2016
Citation
Mutagenesis, 2016, v. 31, n. 6, p. 655-659 How to Cite?
Abstract© 2016 The Author 2016. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Oxidation-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 s ubjects 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.
Persistent Identifierhttp://hdl.handle.net/10722/244058
ISSN
2021 Impact Factor: 2.954
2020 SCImago Journal Rankings: 0.723
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Erica W.-
dc.contributor.authorCollins, Andrew R.-
dc.contributor.authorPang, Marco Y.C.-
dc.contributor.authorSiu, Parco P.M.-
dc.contributor.authorLai, Claudia K.Y.-
dc.contributor.authorWoo, Jean-
dc.contributor.authorBenzie, Iris F.F.-
dc.date.accessioned2017-08-31T08:55:55Z-
dc.date.available2017-08-31T08:55:55Z-
dc.date.issued2016-
dc.identifier.citationMutagenesis, 2016, v. 31, n. 6, p. 655-659-
dc.identifier.issn0267-8357-
dc.identifier.urihttp://hdl.handle.net/10722/244058-
dc.description.abstract© 2016 The Author 2016. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. Oxidation-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 s ubjects 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.-
dc.languageeng-
dc.relation.ispartofMutagenesis-
dc.titleVitamin D and oxidation-induced DNA damage: Is there a connection?-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/mutage/gew033-
dc.identifier.scopuseid_2-s2.0-84994476628-
dc.identifier.volume31-
dc.identifier.issue6-
dc.identifier.spage655-
dc.identifier.epage659-
dc.identifier.eissn1464-3804-
dc.identifier.isiWOS:000388015700005-
dc.identifier.issnl0267-8357-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats