Gold R L, Anderson R R, Natoli V D, Gange R W
Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston 02114.
J Invest Dermatol. 1988 Jun;90(6):818-22. doi: 10.1111/1523-1747.ep12462047.
Suberythemogenic exposure of human skin treated with aqueous 8-MOP to radiation greater than 380 nm prolongs photosensitization to subsequent UVA from 6 to 24-72 h. One hypothesis for prolonged photosensitization is that greater than 380 nm irradiation forms 8-MOP-DNA monoadducts, which are removed more slowly than free 8-MOP and serve as a substrate for crosslinking by further UVA exposure. Sufficient DNA crosslinking results in erythema. We have examined this hypothesis by measuring the action spectrum for induction of prolonged photosensitization. Skin of normal volunteers was treated with aqueous 8-MOP (0.003%) and immediately received suberythemogenic monochromatic exposures between 334 and 430 nm. twenty-four hours later, the presence of prolonged sensitization was tested by small exposures of UVA. Erythema was evaluated 3 and 5 d later, and an action spectrum for prolonged sensitization was determined. The minimum phototoxic dose (MPD) was also determined at each wavelength. The action spectrum for prolonged photosensitization declined gradually between 334 and 425 nm. The action spectrum for delayed erythema induced by a single exposure of 8-MOP-treated skin declined rapidly from 334-390 nm. These findings are consistent with prolonged binding of 8-MOP in the skin by an initial exposure, possibly as 8-MOP-DNA monoadducts, allowing the second exposure to induce an erythemogenic event, possibly crosslinking of DNA.
用8-甲氧基补骨脂素水溶液处理过的人体皮肤，在接受大于380 nm的辐射后发生亚红斑反应，会使随后对UVA的光敏化时间从6小时延长至24 - 72小时。关于光敏化时间延长的一种假说是，大于380 nm的辐射会形成8-甲氧基补骨脂素-DNA单加合物，其清除速度比游离的8-甲氧基补骨脂素慢，并且作为进一步UVA照射导致交联的底物。足够的DNA交联会导致红斑。我们通过测量诱导光敏化时间延长的作用光谱来检验这一假说。正常志愿者的皮肤用8-甲氧基补骨脂素水溶液（0.003%）处理，然后立即接受334至430 nm之间的亚红斑单色照射。24小时后，通过小剂量UVA照射来测试是否存在延长的致敏作用。在3天和5天后评估红斑情况，并确定延长致敏作用的作用光谱。同时还在每个波长下测定了最小光毒性剂量（MPD）。延长光敏化的作用光谱在334至425 nm之间逐渐下降。单次8-甲氧基补骨脂素处理的皮肤诱导延迟红斑的作用光谱在334 - 390 nm之间迅速下降。这些发现与最初照射使8-甲氧基补骨脂素在皮肤中长时间结合一致，可能是以8-甲氧基补骨脂素-DNA单加合物的形式，从而使第二次照射引发红斑反应，可能是DNA交联。
