BACKGROUND: Sun exposure is accepted as the major risk factor for developing skin cancer, the most common cancer in the western world. Ultraviolet-B (UV-B) radiation is considered the causative agent, but recently several findings suggest a role also for ultraviolet-A (UV-A) radiation. Repeated suberythemal doses of ultraviolet-A1 (UV-A1) on healthy human skin induce an increase of p53 immunoreactive cells in epidermis, which may indicate cell cycle arrest and/or occurrence of p53 mutations.
METHODS: We have investigated the possible mutagenic effect of UV-A1 on skin by sequencing exons 4-11 and adjacent intron sequence of the p53 gene in immunoreactive single cells from three healthy individuals. Previously unexposed buttock skin was irradiated three times a week for 2 weeks with physiological fluences (40 J/cm2) of UV-A1. Punch biopsies were taken before and at different time-points after the exposure, and from these single p53 immunoreactive cells were isolated by using laser-assisted microdissection.
RESULTS: Three mutations--all being indicative of oxidative damage and most likely related to UV-A exposure--were found among the 37 single cells from exposed skin, whereas no mutations were found in the 22 single cells taken before exposure.
CONCLUSIONS: The findings indicate a mutagenic effect of low-dose UV-A1 on healthy human skin, which further demonstrates the importance of considering UV-A when taking protective measures against skin cancer.
BACKGROUND: Ultraviolet B (UVB) radiation increases the serum level of 25-hydroxyvitamin D [25(OH)D]. However, the impact of UVA on vitamin D synthesis by UVB is poorly understood clinically.
OBJECTIVE: To examine how different combinations of UVA and UVB radiation affect S-25(OH)D for the same vitamin D-weighted exposure.
MATERIALS AND METHODS: Healthy participants were recruited and subsequently divided into four comparable groups regarding initial 25(OH)D value. The different radiations given were whole-body UVB (n = 23), UVAB (n = 23) and UVA (n = 10). The controls (n = 19) had no intervention. The exposure times were chosen to give the same calculated vitamin D effective dose (suberythemal exposures ≤1 standard erythema dose). Blood samples were collected before the first irradiation (t0), immediately after the last (fifth) irradiation (t1) and then after another 2 days after the last (fifth) irradiation (t2).
RESULTS: UVB and UVAB radiation significantly increased 25(OH)D levels. In the UVA group the increase was less with the same vitamin D-weighted radiation dose.
CONCLUSIONS: Short sessions of UVB or UVAB radiation with the same vitamin D-weighted exposure increased 25(OH)D levels. The UVA dose does not influence 25(OH)D levels under short exposure times. However, there was a significantly lower increase of 25(OH)D levels during longer UVA irradiation (≥9 min).
BACKGROUND: Ultraviolet radiation (UVR) has a variety of effects on human skin. Best known are the effects of UVB (290-320 nm) and UVA2 (320-340 nm), which cause DNA damage and increased risk of cancer. However, the effects of UVA1 (340-400 nm) have been not completely investigated.
METHODS: The effects of repetitive low doses of UVA1 and visible light were studied in 12 healthy individuals. A part of the buttock was exposed to 20 J/cm2 UVA1 and another part of 126 J/cm2 of visible light three times a week for 4 weeks. Repeated punch biopsies were taken during the 4 weeks of treatment and also 2 weeks after the last irradiation. The avidin-biotin-immunoperoxidase technique was used to investigate the expression of p53, p21WAF, bcl-2, Ki67 and cyclin A.
RESULTS: By comparison to untreated skin, an increased expression of p53 but not p21WAF in keratinocytes was seen. The bcl-2 protein expression increased slightly after both UVA1 and visible light. An increased staining with Ki67 and cyclin A after UVA1 but not after visible light was observed as a sign of increased proliferation.
CONCLUSION: These results suggest that suberythemal doses of UVA1 and even visible light may cause DNA damage.
Solar urticaria is characterized by itching weals that occur a few minutes after exposure to visible or ultraviolet light. The symptoms may sometimes restrict normal daily life. Treatment is difficult in more severe cases. We describe one patient with solar urticaria who was successfully treated with cyclosporin A. The patient had first been treated with antihistamine, PUVA and chloroquine phosphate without effect. Cyclosporin was given in a dose of 4.5 mg/kg body weight/day. Phototesting before, during and after treatment showed a decreased light sensitivity to UVA, UVB and visible light during cyclosporin treatment compared with phototesting before therapy. The patient could be out in the sun for at least 1 h with minimal urticaria during cyclosporin therapy compared with only a few minutes previously. However, 1-2 weeks after cyclosporin therapy was discontinued, skin symptoms returned. Cyclosporin therapy is a possible treatment in severe cases of solar urticaria where other treatments have failed, especially in countries where treatment is necessary only for a few months during summer.