Bishop S C, Abel E A
Arch Dermatol Res. 1985;278(1):25-30. doi: 10.1007/BF00412491.
The skin of patients receiving psoralen and UVA (PUVA) therapy for psoriasis is exposed to trace amounts of UVB radiation emitted by PUVA irradiators in addition to UVA. DNA repair activity was measured using autoradiography in the uninvolved skin of PUVA-treated patients in order to determine whether 8-methoxypsoralen (8-MOP) plus UVA elicits repair, inhibits the skin repair response to UVB, or protects epidermal-cell DNA from UVB damage by promoting a tan. Epidermal-DNA repair activity was observed in 27 out of 37 patients following the first PUVA treatment. Phototesting with multiples of the initial UV dose elicited a linear increase in repair activity. Glass-filtered radiation failed to stimulate repair, indicating that the reaction was due to UVB, not to 8-MOP plus UVA. The same amount of repair activity was observed in the skin of patients irradiated either before or after 8-MOP ingestion, demonstrating that the drug did not interfere with the response of the skin to UVB. At clearing, however, the repair activity was never greater than that elicited at the initial treatment and was often undetectable despite a tenfold increase in UV exposure. It is proposed that DNA damage should be measured to determine whether epidermal cells are entirely protected from UVB radiation at the completion of therapy.
接受补骨脂素和长波紫外线（PUVA）治疗银屑病的患者皮肤，除了暴露于长波紫外线外，还会受到PUVA照射器发出的微量中波紫外线辐射。为了确定8-甲氧基补骨脂素（8-MOP）加UVA是否引发修复、抑制皮肤对中波紫外线的修复反应，或通过促进晒黑来保护表皮细胞DNA免受中波紫外线损伤，采用放射自显影法测量了接受PUVA治疗患者未受累皮肤的DNA修复活性。37例患者中，27例在首次PUVA治疗后观察到表皮DNA修复活性。用初始紫外线剂量的倍数进行光试验，可使修复活性呈线性增加。经玻璃滤光片过滤的辐射未能刺激修复，表明该反应是由中波紫外线引起的，而非8-MOP加UVA。在摄入8-MOP之前或之后接受照射的患者皮肤中观察到相同程度的修复活性，表明该药物不会干扰皮肤对中波紫外线的反应。然而，在皮损消退时，修复活性从未高于初始治疗时引发的活性，尽管紫外线暴露增加了10倍，但修复活性通常仍检测不到。建议测量DNA损伤，以确定在治疗结束时表皮细胞是否完全免受中波紫外线辐射。
