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大鼠肝脏制剂体外对三氯氟甲烷的厌氧脱氯作用。

The anaerobic dechlorination of trichlorofluoromethane by rat liver preparations in vitro.

作者信息

Wolf C R, King L J, Parke D V

出版信息

Chem Biol Interact. 1978 Jun;21(2-3):277-88. doi: 10.1016/0009-2797(78)90026-1.

DOI:10.1016/0009-2797(78)90026-1
PMID:28182
Abstract

Incubation of trichlorofluoromethane with a liver microsomal fraction and an NADPH generating system under anaerobic conditions produced a metabolite dichlorofluoromethane, characterised by gas chromatography and mass spectrometry. The metabolic reaction was carried out by liver microsomes from the mouse, rabbit, hamster and rat and was increased by phenobarbitone pre-treatment. The formation of dichlorofluoromethane in vitro was enhanced by the addition of FMN, but partially inhibited by the presence of air, oxygen, SK&F 525-A, metyrapone and carbon tetrachloride and totally inhibited by carbon monoxide. The consumption of NADPH in the reaction was greater than could be accounted for by the production of dichlorofluoromethane indicating the possible formation of other metabolic products. It is suggested that trichlorofluoromethane interacts with the reduced form of cytochrome P-450 at the oxygen binding site and a possible mechanism for its subsequent reductive dechlorination is proposed.

摘要

在厌氧条件下,将三氯氟甲烷与肝微粒体部分及一个NADPH生成系统一起温育,产生了一种代谢产物二氯氟甲烷,通过气相色谱和质谱对其进行了表征。该代谢反应由来自小鼠、兔子、仓鼠和大鼠的肝微粒体进行,且经苯巴比妥预处理后反应增强。体外二氯氟甲烷的形成因添加FMN而增强,但因空气、氧气、SK&F 525 - A、甲吡酮和四氯化碳的存在而部分受到抑制,因一氧化碳而完全受到抑制。反应中NADPH的消耗大于二氯氟甲烷生成所能解释的量,这表明可能形成了其他代谢产物。有人提出,三氯氟甲烷在氧结合位点与细胞色素P - 450的还原形式相互作用,并提出了其随后进行还原脱氯的一种可能机制。

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