1. ¹Department of Physiology and The Bosch Institute, University of Sydney, Sydney, New South Wales, Australia
2. ²Department of Medicine (Dermatology), University of Sydney, Sydney, New South Wales, Australia
3. ³Faculty of Veterinary Science, University of Sydney, Sydney, New South Wales, Australia

Correspondence: Dr Rebecca S. Mason, Department of Physiology and The Bosch Institute, University of Sydney, Sydney, New South Wales 2006, Australia. E-mail: rebeccam@physiol.usyd.edu.au

⁴Joint first authors

Received 23 March 2006; Revised 31 July 2006; Accepted 18 August 2006; Published online 14 December 2006.

Abstract

Vitamin D is produced in skin by UVB radiation (290–320 nm) acting on 7-dehydrocholesterol. The hypotheses that the active vitamin D hormone, 1,25 dihydroxyvitamin D₃ (1,25(OH)₂D₃), would increase the survival of skin cells after UV irradiation and that surviving cells after 1,25(OH)₂D₃ treatment would have no increase in DNA damage were tested. The survival of keratinocytes post-UVR was significantly greater after treatment with 1,25(OH)₂D₃ compared to vehicle (P<0.01). Significant reductions in thymine dimers (TDs) in surviving keratinocytes after UVR were noted in the presence of 1,25(OH)₂D₃ (P<0.001). Nuclear p53 protein expression increased after UVR and was significantly higher in keratinocytes treated with 1,25(OH)₂D₃ (P<0.01), whereas NO products were significantly reduced (P<0.05). Both the increase in nuclear accumulation of p53 protein and reduced formation of nitric oxide products may contribute to the reduction in TDs seen with 1,25(OH)₂D₃ after UVR. Reductions in numbers of sunburn cells (P<0.01) and in TDs (P<0.05) were observed 24 hours after UVR in skin sections from Skh:hr1 mice treated with 1,25(OH)₂D₃. These results are consistent with the proposal that the vitamin D system in skin may be part of an intrinsic protective mechanism against UV damage.