Iris Benzie
The Hong Kong Polytechnic University, Hong Kong
Title: Vitamin D Status in apparently healthy young adults in Hong Kong
Biography
Biography: Iris Benzie
Abstract
BACKGROUND: Oxidation-induced damage to DNA increases when antioxidant defences or base excision repair is inadequate. Increased DNA damage can lead to mutagenic changes, apoptosis and loss of cellular function, all of which increase risk of non-communicable diseases (NCDs). There is increasing observational evidence linking vitamin D deficiency to increased risk of various NCDs, including cancer, coronary heart disease, dementia and diabetes. Cell culture studies have shown that vitamin D protects DNA from UV- and oxidation- induced damage, but human studies are lacking. HYPOTHESIS AND AIM: We hypothesize that lower vitamin D status associates with higher levels of oxidation-induced DNA damage in humans. This study aimed to investigate this. METHOD: The Fpg-assisted comet (single cell gel electrophoresis) assay was used to measure oxidation-induced DNA damage (as %DNA in comet tail) in peripheral lymphocytes from healthy, young (18-26 years; n=173) volunteers. Vitamin D status was assessed as plasma 25(OH)D, measured by LC-MS/MS. Here we present preliminary results from 49 of the 173 subjects. Correlational analysis (Spearman’s) was performed; differences across tertiles of 25(OH)D were explored using ANOVA. RESULTS: Mean(SD)%DNA in comet tail was 21.0(2.9)%; mean(SD) 25(OH)D was 46.7(13.3)nmol/l [range 25.9-84.3]. Mean(SD) values for %DNA in comet tail across 25(OH)D tertiles (n=~16/tertile) were 20.7(2.4)%, 20.9(2.5)%, and 21.5(3.6)% (p>0.05). No significant correlation was seen between 25(OH)D and oxidation-induced damage to lymphocytic DNA. CONCLUSION: Our hypothesis that poor vitamin D status associates with higher levels of oxidation-induced DNA damage is not supported by these preliminary data from 49 healthy young adults. The study is continuing.