MECHANISMS OF CHEMICALLY INDUCED PHOTOSENSITIVITY

已知光与内源或外源化学物质相互作用 皮肤或眼睛，以产生光敏作用(光毒性或 光过敏)。虽然所有形式的光敏性的初始步骤 必须是化学物质或其代谢物对光的吸收 致敏的确切机制尚不清楚。这样做的目的是 研究是确定光诱导的自由基或活性氧 物种在光敏作用中起着重要作用。氯丙嗪(CPZ)是一种 同时引起光毒和光过敏的抗精神病药物 反应。CPZ在水溶液中的紫外光照射导致 碳-氯键的均解断裂和An的生成 从合适的给体中提取氢原子的芳基。CPZ 在280 nm处照射时也发生光电离，得到CPZ阳离子 激进的。因此，似乎不太可能涉及CPZ阳离子自由基 这种药物的光毒性。CPZ产生的单线态氧 (1270 nm的磷光)在苯、正己烷和 环己烷，但不在水溶液或酒精溶液中。CPZ亚硫醚， 在人类和其他哺乳动物物种中形成的，产生了 近紫外光照射下的羟基自由基和CPZ阳离子自由基 灯。血卟啉衍生物(HPD)和光将氧气转化为 在光存在的情况下，羟基自由基和过氧化氢。HPD 光还引发了硫基自由基的氧依赖形成 来自半胱氨酸。卤代水杨胺。 3，3‘，4’，5-四氯水杨基苯胺(TCSA)，3，4‘，5-三溴水杨基苯胺， (TBSA)和N-丁基-4-氯水杨基苯胺(布洛沙胺)均生成芳基 光脱卤化过程中产生的自由基。谷胱甘肽对牛血清白蛋白的辐照 或半胱氨酸导致相应硫基的生成 激进分子。因此，这些人的皮肤光过敏似乎是可能的 化合物可能是由于这些自由基与蛋白质反应而产生的 形成抗原。

Light is known to interact with endogenous or exogenous chemical agents in the skin or eyes, to produce photosensitization (phototoxicity or photoallergy). While the initial step in all forms of photosensitivity must be the absorption of light by the chemical or its metabolites, the precise mechanisms of sensitization are unknown. The objective of this study is to determine whether light-induced free radicals or active oxygen species play a role in photosensitization. Chlorpromazine (CPZ) is an antipsychotic drug that causes both phototoxic and photoallergic reactions. UV irradiation of CPZ in aqueous solution resulted in the homolytic cleavage of the carbon-chlorine bond and the generation of an aryl radical which extracted a hydrogen atom from suitable donors. CPZ also photo-ionized when irradiated at 280 nm to give the CPZ cation radical. Thus, it appears unlikely that the CPZ cation radical is involved in the phototoxicity of this drug. CPZ generated singlet oxygen (phosphorescence at 1270 nm) when irradiated in benzene, hexane and cyclohexane but not in aqueous or alcoholic solutions. The CPZ sulfoxide, which is formed in humans and other mammalian species, generated the hydroxyl radical and CPZ cation radical upon irradiation with near UV light. Hematoporphyrin derivative (HPD) and light convert oxygen to hydroxyl free radical and hydrogen peroxide in the presence of light. HPD and light also initiated an oxygen-dependent formation of thiyl radical from cysteine. Halogenated salicylanilides eg. 3,3',4',5-tetrachlorosalicylanilide (TCSA), 3,4',5-tribromosalicylanilide, (TBSA) and N-butyl-4-chlorosalicylanilide (buclosamide) all generated aryl radicals during photodehalogenation. Irradiation of TBSA with glutathione or cysteine resulted in the generation of the corresponding thiyl radicals. Thus, it appears possible that the skin photoallergy of these compounds may result from the reaction of these radicals with proteins to form antigens.