Prolonged skin photosensitization induced by methoxsalen and subphototoxic UVA irradiation.
Prolonged skin photosensitization induced by methoxsalen and subphototoxic UVA irradiation.
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甲氧沙林和亚光毒性 UVA 照射引起的长时间皮肤光敏化。
DOI：
10.1111/1523-1747.ep12260043
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Parrish,JA
中科院分区：
文献类型：
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作者：
Gange,RW;Levins,P;Murray,J;Anderson,RR;Parrish,JA
局部使用8-甲氧补骨脂素（8-MOP）可短暂提供足以产生明显皮肤光敏作用的游离补骨脂素，但最初仅输送小剂量的UVA，以产生许多单加合物，但很少产生交联。在清除剩余的游离补骨脂素足够的时间后，进行第二次UVA暴露。第二次暴露不应在不存在游离peptide的情况下产生任何额外的单加合物，但剩余的单加合物可转化为交联。当存在游离8- MOP时，观察到由先前给予的非常小剂量的UVA引起的延长的持续UVA-光敏状态，这强烈地表明，紫杉醇-DNA交联本身引发了8-MOP对皮肤的大部分光毒性作用，并且单加合物诱导的急性炎症反应少得多。因为红斑是作为终点研究的，所以数据没有说明单加合物与交联在引起诱变、色素沉着过度、治疗或其他皮肤反应方面的相对贡献。对诱导的持续光敏状态的其他解释也是可能的，但不太站得住脚或完全是假设。
Topical 8-methoxypsoralen (8-MOP) was used to briefly provide free psoralen sufficient for marked cutaneous photosensitization, but only a small dose of UVA was delivered initially, in an effort to produce many monoadducts but few crosslinks. After ample time for clearance of the remaining free psoralen a second UVA exposure was delivered. The second exposure should not have generated any additional monoadducts in the absence of free psoralen, but the remaining monoadducts could be converted to crosslinks. The observation of a prolonged persistent UVA-photosensitive state caused by prior, very small doses of UVA given while free 8- MOP was present strongly suggests that psoralen-DNA crosslinks per se initiate much of the phototoxic effect of 8-MOP on skin, and that monoadducts induce much less acute inflammatory response. Because erythema was studied as the end point, the data say nothing about relative contributions of monoadducts vs crosslinks in causing mutagenesis, hyperpigmentation, therapeutic or other cutaneous responses. Other explanations for the induced persistent photosensitive state are also possible, but less tenable or entirely hypothetical.