Photosensitization reactions have been demonstrated to be largely responsible for the deleterious biological effects of UV and visible radiation, as well as for the curative actions of photomedicine. A large number of endogenous and exogenous photosensitizers, biological targets and mechanisms have been reported in the past few decades. Evolving from the original definitions of the type I and type II photosensitized oxidations, we now provide physicochemical frameworks, classifications and key examples of these mechanisms in order to organize, interpret and understand the vast information available in the literature and the new reports, which are in vigorous growth. This review surveys in an extended manner all identified photosensitization mechanisms of the major biomolecule groups such as nucleic acids, proteins, lipids bridging the gap with the subsequent biological processes. Also described are the effects of photosensitization in cells in which UVA and UVB irradiation triggers enzyme activation with the subsequent delayed generation of superoxide anion radical and nitric oxide. Definitions of photosensitized reactions are identified in biomolecules with key insights into cells and tissues.

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生物分子的光敏化反应：定义、目标和机制

光敏反应已被证明是造成紫外线和可见光辐射的有害生物效应以及光医学的治疗作用的主要原因。在过去的几十年中，已经报道了大量的内源性和外源性光敏剂、生物靶点和机制。从 I 型和 II 型光敏氧化的原始定义演变而来，我们现在提供这些机制的物理化学框架、分类和关键示例，以便组织、解释和理解文献和新报告中可用的大量信息，这些信息是在蓬勃发展中。本综述以扩展的方式调查了所有已确定的主要生物分子组（如核酸、蛋白质、脂质弥合了随后的生物过程的差距。还描述了细胞中光敏化的影响，其中 UVA 和 UVB 照射触发酶活化，随后延迟产生超氧阴离子自由基和一氧化氮。光敏反应的定义是在生物分子中确定的，具有对细胞和组织的关键见解。