title: Vitamin D and oxidation-induced DNA damage: is there a connection?
abstract: 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 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.
authors.forename: Erica W
authors.initials: EW
authors.lastname: Wang
authors.affiliation: Department of Nutrition, The University of Oslo, PO Box 1072, Blindern, 0316 Oslo, Norway.
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Collins
authors.affiliation: Department of Rehabilitation Sciences and.
authors.forename: Marco Y C
authors.initials: MY
authors.lastname: Pang
authors.forename: Parco P M
authors.initials: PP
authors.lastname: Siu
authors.affiliation: School of Nursing, The Hong Kong Polytechnic University, Yuk Choi Road, Kowloon, Hong Kong and.
authors.forename: Claudia K Y
authors.initials: CK
authors.lastname: Lai
authors.affiliation: Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong.
authors.forename: Jean
authors.initials: J
authors.lastname: Woo
authors.forename: Iris F F
authors.initials: IF
authors.lastname: Benzie
mesh_terms: D000293:Adolescent; D000328:Adult; D020552:Comet Assay; D004249:DNA Damage; D043382:DNA-Formamidopyrimidine Glycosylase; D029968:Escherichia coli Proteins; D005260:Female; D006801:Humans; D008297:Male; D018384:Oxidative Stress; D014807:Vitamin D / Q000097:blood*; D055815:Young Adult
chemical_list: D029968:Escherichia coli Proteins; D014807:Vitamin D; D043382:DNA-Formamidopyrimidine Glycosylase; C468610:DNA-formamidopyrimidine glycosylase, E coli