Sunlight and vitamin D affect DNA damage, cell division and cell death in human lymphocytes: a cross-sectional study in South Australia
Visalini Nair-Shalliker1,2,firstname.lastname@example.org, Michael Fenech3, Peta M. Forder4,5, Mark S. Clements6,7 and Bruce K. Armstrong1
1 Sydney School of Public Health, The University of Sydney, Sydney, New South Wales 2006, Australia
2 Cancer Epidemiology Research Unit, Cancer Council New South Wales, Sydney, New South Wales 2011, Australia
3 CSIRO Food and Nutritional Sciences, PO Box 10041, Adelaide, South Australia 5000, Australia
4 NHMRC Clinical Trials Centre, The University of Sydney, Sydney, New South Wales 2006, Australia
5 Research Centre for Gender, Health and Aging, Faculty of Health, University of Newcastle, Newcastle, New South Wales, 2300, Australia
6 National Centre for Epidemiology and Population Health, The Australian National University, Canberra, ACT 0200, Australia
7 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Sweden
Mutagenesis (2012) doi: 10.1093/mutage/ges026,
The ultraviolet (UV)-B spectrum in solar UV radiation is essential for stimulating the epidermal production of vitamin D but also damages DNA and causes cancer in exposed cells. We examined the role of solar UV in inducing DNA damage in blood lymphocytes and the possible modulation of this damage by serum 25-hydroxy vitamin D (25(OH)D) in 207 male and female participants from South Australia.
Personal solar UV exposure was estimated from hours of outdoor exposure recalled at the time of blood collection for analysis of DNA damage in lymphocytes, using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay and of serum 25(OH)D. We examined the association between solar UV exposure, serum 25(OH)D and DNA damage using multiple linear regression, with age, sex, body mass index and alcohol consumption as covariates.
The frequency of cells with micronuclei (a biomarker of chromosome breakage or loss) increased with increasing sun exposure [% increase = 5.24; 95% confidence interval (CI): 0.35 to 10.37 P-value = 0.04]
but cells with nucleoplasmic bridges (a biomarker of misrepair of DNA strand breaks or telomere end fusions) decreased (% increase = ?8.38; 95% CI: ?14.32 to ?2.03 P-value = 0.01).
There was also a fall in the nuclear division index (NDI) (% increase = ?1.01; 95% CI: ?2.00 to 0.00 P-value = 0.05), suggesting diminished mitogenic response and, possibly, immune suppression.
There was no overall relationship between 25(OH)D and DNA damage.
There were, however, weak modulating effects of 25(OH)D on the associations of solar UV exposure with micronucleus formation and with NDI (P-interaction = 0.03 and 0.05, respectively), where the increase in micronuclei and fall in NDI with increasing solar UV were greater at serum 25(OH)D levels <50 nmol/l.
Thus, the influence of solar UV exposure in causing DNA damage or immune suppression in internal tissues may be stronger when vitamin D levels are low.
© The Author 2012. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions at oup.com.
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