Photoprotection by 20-hydroxyvitamin D3, a product of CYP11A1 in skin

Abstract

Skin cancer is one of the most common health issues afflicting people in many countries, particularly in Australia. The major cause of skin cancer is ultraviolet radiation (UV), which is also needed for vitamin D synthesis. There is also evidence from the Mason group that the hormonally active form of vitamin D, 1α,25-hydroxyvitamin D3 (1,25(OH)2D3), provides photoprotection. Studies on the effects of 20(OH)D3 on DNA damage and immunosuppression done in our laboratory by colleagues, revealed that 20(OH)D3 is as effective as 1,25(OH)2D3 in reducing thymine dimer formation and UVR-induced immunosuppression in female hairless Skh:hr1 mice (Tongkao-on et al., 2015). The aim of this project was to explore whether 20-hydroxyvitamin D3 (20(OH)D3), a product of vitamin D3 hydroxylation, provides protection against UV-induced photocarcinogenesis. In order to investigate whether the protection against acute UV-induced damage translates into prevention of skin carcinogenesis, the major, in vivo component of this study involved a 40 week photocarcinogenesis study and contact hypersensitivity (CHS) response experiment, with 1,25(OH)2D3 and 20(OH)D3 applied as topical treatments post UV irradiation. The results from the in vivo study showed that 1,25(OH)2D3 was effective at inhibiting UV-induced tumour formation and progression, but 20(OH)D3 was not observed to be effective in reducing the following parameters: tumour incidence, tumour latency, tumour multiplicity and squamous cell carcinoma (SCC) incidence.