Solar-simulated skin adaptation and its effect on subsequent UV-induced epidermal DNA damage

被引:74
作者
de Winter, S
Vink, AA
Roza, L
Pavel, S
机构
[1] Leiden Univ, Med Ctr, Dept Dermatol, NL-2300 RC Leiden, Netherlands
[2] TNO Voeding, Dept Target Organ Toxicol, Zeist, Netherlands
关键词
cyclobutane thymine dimers; erythema; p53; pigmentation; skin; skin cancer; UV radiation;
D O I
10.1046/j.0022-202x.2001.01478.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Repeated skin exposure to ultraviolet radiation leads to increased tolerance for erythema. Whether this tolerance is accompanied by a significant protection against epidermal DNA injury has never been thoroughly investigated. In a first set of experiments we irradiated 25 healthy volunteers three times a week for 3 wk using solar-simulating tanning lamps. In addition, all individuals were exposed to a (challenge) dose of three times the initial minimal erythema dose on a small area of skin before the first and after the final exposure. On both occasions, cyclobutane pyrimidine dimers were quantified in biopsies. As expected, repeated ultraviolet exposures resulted in increased epidermal pigmentation and thickness. The ultraviolet sensitivity for erythema decreased on average by 75%. The cyclobutane pyrimidine dimer formation was reduced on average by 60%. In a second set of experiments, with a group of 13 subjects, DNA repair kinetics were assessed. Within a period of 5 d after a single, slightly erythemal dose (1.2 minimal erythema dose), levels of cyclobutane pyrimidine dimer and p53-expressing cells were determined in skin biopsies. Both markers of DNA damage were elevated upon the single ultraviolet exposure and returned to background levels after 3-4 d. This information is important when trying to minimize the risk of DNA damage accumulation after repeated exposures during a tanning course.
引用
收藏
页码:678 / 682
页数:5
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