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药物光敏性的分子层面,特别强调补骨脂素光敏化反应。

Molecular aspects of drug photosensitivity with special emphasis on psoralen photosensitization reaction.

作者信息

Pathak M A

出版信息

J Natl Cancer Inst. 1982 Jul;69(1):163-70. doi: 10.1093/jnci/69.1.163.

Abstract

Photosensitization reactions involve phototoxic reactions and photoallergic reactions, which are less common. Common drugs and chemicals that photosensitize humans are listed. Phototoxic reactions include the following: 1) direct photosensitization (type I reactions), in which the reactions of the triplet-state sensitizer are directly attributable to a component other than oxygen (e.g., DNA, proteins, and cell membranes), and 2) indirect photosensitization (type II reactions), in which the triplet state of a sensitizer reacts first with molecular oxygen, producing an "active oxygen" intermediate that subsequently reacts with the biologic system. The active oxygen intermediates are singlet oxygen (1O2)k, superoxide radical anions (O(2), and hydroxy radicals. Psoralen-induced skin photosensitization appears to involve both type I and type II reactions. The formation of monofunctional bifunctional psoralen-DNA photoadducts (a type I reaction) is probably responsible for cell damage, cell death, mutation, and even skin carcinogenesis. The erythema response appears to be the result of a type II reaction.

摘要

光敏反应包括光毒性反应和光变应性反应,后者较为少见。文中列出了可使人类产生光敏反应的常见药物和化学物质。光毒性反应包括以下两种:1)直接光敏化(I型反应),即三重态敏化剂的反应直接归因于除氧以外的成分(如DNA、蛋白质和细胞膜);2)间接光敏化(II型反应),即敏化剂的三重态首先与分子氧发生反应,生成“活性氧”中间体,该中间体随后与生物系统发生反应。活性氧中间体包括单线态氧(1O2)、超氧阴离子自由基(O(2))和羟基自由基。补骨脂素引起的皮肤光敏反应似乎涉及I型和II型反应。单功能和双功能补骨脂素-DNA光加合物的形成(I型反应)可能是导致细胞损伤、细胞死亡(译者注:此处原文cell death前可能多了逗号)、突变甚至皮肤癌发生的原因。红斑反应似乎是II型反应的结果。

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