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萘普生在红细胞中产生光致敏作用的分子机制。

Molecular mechanism of naproxen photosensitization in red blood cells.

作者信息

Costanzo L L, De Guidi G, Condorelli G, Cambria A, Famà M

机构信息

Dipartimento di Scienze Chimiche, Università di Catania, Italy.

出版信息

J Photochem Photobiol B. 1989 Apr;3(2):223-35. doi: 10.1016/1011-1344(89)80064-8.

DOI:10.1016/1011-1344(89)80064-8
PMID:2498486
Abstract

Red blood cell lysis photosensitized by naproxen was investigated. The photohemolysis rate was enhanced by deuterium oxide and inhibited by butylated hydroxyanisole, reduced glutathione, sodium azide and superoxide dismutase. Photohemolysis was also observed under anaerobic conditions. In the absence of red cells the irradiation of deaerated solutions underwent a decarboxylation process via intermediate radicals, while under aerobic conditions photo-oxidation leading to the photoproduct 6-methoxy-2-acetonaphthone occurred. A molecular mechanism involving free radicals and singlet oxygen as important intermediates and consistent with the overall results is proposed.

摘要

研究了萘普生光敏化的红细胞裂解。重水可提高光溶血速率,而丁基化羟基茴香醚、还原型谷胱甘肽、叠氮化钠和超氧化物歧化酶则抑制光溶血速率。在厌氧条件下也观察到了光溶血现象。在没有红细胞的情况下,脱气溶液的辐照通过中间自由基进行脱羧过程,而在有氧条件下会发生光氧化反应生成光产物6-甲氧基-2-乙酰萘。提出了一种涉及自由基和单线态氧作为重要中间体且与总体结果一致的分子机制。

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