PHOTO-TOXICITY MECHANISMS - CHLORPROMAZINE PHOTOSENSITIZED DAMAGE TO DNA AND CELL-MEMBRANES
PHOTO-TOXICITY MECHANISMS - CHLORPROMAZINE PHOTOSENSITIZED DAMAGE TO DNA AND CELL-MEMBRANES
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DOI：
10.1111/1523-1747.ep12479244
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发表时间：
1981-01-01
影响因子：
6.5
通讯作者：
KOCHEVAR, IE
中科院分区：
文献类型：
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作者：
KOCHEVAR, IE
生物分子的光敏损伤是光毒性反应的起始过程。现在认识到，许多光毒性化合物可以光敏损伤一种以上类型的生物基板。光毒性化合物与DNA、可溶性蛋白质和膜组分的体外光引发反应可按其分子机制分类：（1）其中光毒性化合物的激发态（2）其中衍生自光毒性化合物的分子（或衍生自其的不稳定物质）直接与生物底物反应的那些（光产物或活性氧物质）与生物底物反应。本文介绍了氯丙嗪光敏损伤细胞膜，蛋白质和DNA的机制，并比较它们的光敏机制由peptiens，卟啉，染料，和其他分子。
Photosensitized damage to biological molecules is the initial process in phototoxic responses. It is now recognized that many phototoxic compounds can photosensitize damage to more than one type of biological substrate. Thein vitrolight-initiated reactions of phototoxic compounds with DNA, soluble proteins and membrane components can be classified by their molecular mechanisms: (1) those in which an excited state of the photo-toxic compound (or an unstable species derived from it) reacts directly with the biological substrate and (2) those in which a molecule derived from the phototoxic compound (a photoproduct or an activated oxygen species) reacts with the biological substrate. This paper describes the mechanisms by which chlorpromazine photosensitizes damage to membranes, protein and DNA and compares them to the mechanisms of photosensitization by psoralens, porphyrins, dyes, and other molecules.