High oral vitamin D intake does not protect against UVR-induced squamous cell carcinoma in hairless mice

Background/Aim: The role of vitamin D in skin carcinogenesis is unclear. Vitamin D compounds may play a role in protection against UVR-induced DNA damage, immune suppression and skin carcinogenesis. However, epidemiological studies have also shown an increased incidence of skin cancer associated with high levels of serum vitamin D. The aim was to investigate the influence of vitamin D supplementation on vitamin D levels in the serum, skin, and tumor and on skin cancer development in hairless immunocompetent mice. Materials and Methods: Female C3.Cg-Hrhr/TifBomTac immunocompetent mice (n=125) were randomly allocated into five groups. Two groups received diet enriched with vitamin D₃ corresponding to ~1,200 IU/day or 30 μg/day per mouse. One group received medium enriched vitamin D3 (~600 IU/day or 15 μg/day per mouse). The last two groups received standard diet (~1.2 IU/day or 0.03 μg/day/mouse). Three standard erythema doses (SED) of UVR were given to three groups three times per week, one from each supplementation group. Results: Animals supplemented with high vitamin D₃ had about 150 times higher levels of serum vitamin D3 (p=0.00031) and 3 times higher 25(OH)D₃ serum levels (p=0.00016) than standard diet. Serum vitaminD3 levels in mice supplemented with a medium dose of vitamin D₃ were 18 times higher than those supplemented with standard diet, and 2.3 times higher for 25(OH)D₃ (p=0.00067). All UVR-exposed mice developed tumors. High and medium supplementation of vitamin D₃ did not influence the time to tumor development (p>0.05). Conclusion: This study showed that it was possible to raise vitamin D levels in the serum, skin, and tumors of mice by supplementation, but it did not affect the time to UVR-induced skin cancer.