Felton S J, Cooke M S, Kift R, Berry J L, Webb A R, Lam P M W, de Gruijl F R, Vail A, Rhodes L E
Dermatology Research Centre, Institute of Inflammation and Repair, Faculty of Medical and Human Sciences, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, U.K.
Oxidative Stress Group, Department of Environmental and Occupational Health, Florida International University, Miami, FL, U.S.A.
Br J Dermatol. 2016 Dec;175(6):1320-1328. doi: 10.1111/bjd.14863. Epub 2016 Nov 18.
The concurrent impact of repeated low-level summer sunlight exposures on vitamin D production and cutaneous DNA damage, potentially leading to mutagenesis and skin cancer, is unknown.
This is an experimental study (i) to determine the dual impact of repeated low-level sunlight exposures on vitamin D status and DNA damage/repair (via both skin and urinary biomarkers) in light-skinned adults; and (ii) to compare outcomes following the same exposures in brown-skinned adults.
Ten white (phototype II) and six South Asian volunteers (phototype V), aged 23-59 years, received 6 weeks' simulated summer sunlight exposures (95% ultraviolet A/5% ultraviolet B, 1·3 standard erythemal doses three times weekly) wearing summer clothing exposing ~35% body surface area. Assessments made were circulating 25-hydroxyvitamin D [25(OH)D], immunohistochemistry for cyclobutane pyrimidine dimer (CPD)-positive nuclei and urinary biomarkers of direct and oxidative (8-oxo-deoxyguanosine) DNA damage.
Serum 25(OH)D rose from mean 36·5 ± 13·0 to 54·3 ± 10·5 nmol L (14·6 ± 5·2 to 21·7 ± 4·2 ng mL ) in phototype II vs. 17·2 ± 6·3 to 25·5 ± 9·5 nmol L (6·9 ± 2·5 to 10·2 ± 3·8 ng mL ) in phototype V (P < 0·05). Phototype II skin showed CPD-positive nuclei immediately postcourse, mean 44% (range 27-84) cleared after 24 h, contrasting with minimal DNA damage and full clearance in phototype V (P < 0·001). The findings did not differ from those following single ultraviolet radiation (UVR) exposure. Urinary CPDs remained below the detection threshold in both groups; 8-oxo-deoxyguanosine was higher in phototype II than V (P = 0·002), but was unaffected by UVR.
Low-dose summer sunlight exposures confer vitamin D sufficiency in light-skinned people concurrently with low-level, nonaccumulating DNA damage. The same exposures produce minimal DNA damage but less vitamin D in brown-skinned people. This informs tailoring of sun-exposure policies.
夏季反复低强度阳光照射对维生素D生成和皮肤DNA损伤的同时影响尚不清楚，这可能会导致诱变和皮肤癌。
本实验研究旨在：（i）确定反复低强度阳光照射对浅肤色成年人维生素D状态和DNA损伤/修复（通过皮肤和尿液生物标志物）的双重影响；（ii）比较深肤色成年人相同照射后的结果。
10名年龄在23 - 59岁的白人（II型光皮肤型）和6名南亚志愿者（V型光皮肤型），穿着夏季服装，暴露约35%的体表面积，接受为期6周的模拟夏季阳光照射（95%紫外线A/5%紫外线B，每周3次，每次1.3标准红斑剂量）。评估指标包括循环25-羟基维生素D [25(OH)D]、环丁烷嘧啶二聚体（CPD）阳性细胞核的免疫组织化学检测以及直接和氧化（8-氧代脱氧鸟苷）DNA损伤的尿液生物标志物。
II型光皮肤型血清25(OH)D从平均36.5±13.0 nmol/L（14.6±5.2 ng/mL）升至54.3±10.5 nmol/L（21.7±4.2 ng/mL），而V型光皮肤型从17.2±6.3 nmol/L（6.9±2.5 ng/mL）升至25.5±9.5 nmol/L（10.2±3.8 ng/mL）（P < 0.05）。II型光皮肤型皮肤在照射后立即出现CPD阳性细胞核，24小时后平均清除率为44%（范围27 - 84），而V型光皮肤型DNA损伤最小且完全清除（P < 0.001）。这些结果与单次紫外线辐射（UVR）照射后的结果无差异。两组尿液CPD均低于检测阈值；II型光皮肤型的8-氧代脱氧鸟苷高于V型光皮肤型（P = 0.002），但不受UVR影响。
低剂量夏季阳光照射可使浅肤色人群获得充足的维生素D，同时伴有低水平、无累积的DNA损伤。相同照射对深肤色人群产生的DNA损伤最小，但维生素D生成较少。这为制定日晒政策提供了依据。
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