Bianca Y. McCarthy, Katie M. Dixon, Gary M. Halliday, Vivienne E. Reeve and Rebecca S. Mason Pages 137 - 151 ( 15 )
Sunlight has the potential to induce DNA damage in the skin. If these photolesions are left unrepaired, they can greatly increase the risk of skin cancer. This process is facilitated by another UV-induced insult, photoimmune suppression. Vitamin D metabolites have demonstrated a marked ability to mitigate these negative effects. The photoprotective pathway still remains elusive. Recent research, however, points to the important role of the vitamin D receptor and the endoplasmic reticulum protein ERp57 in mediating the actions of vitamin D compounds. Determining the functional relationship between vitamin D metabolites, the VDR/ERp57 complex, and downstream DNA repair mechanisms will contribute to the greater understanding of this photoprotective system. Furthermore, in light of evidence suggesting that CYP27B1 is not necessary for photoprotection, strong emphasis must now be placed on examining other vitamin D metabolic pathways and the actions of new metabolites in photoprotection. Recent literature points to 20(OH)D3 as a possible alternative to 1,25(OH)2D3. However, further work must be conducted to determine the photoprotective pathway of this vitamin D derivative.
1, 25-dihydroxyvitaminD3, 20-hydroxyvitamin D3, photoprotection, DNA damage, photoimmune suppression, VDR, ERp57.
Department of Physiology and Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW, 2006, Australia.