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抗炎药物:作为自由基活性的体外生物学指标对一种细菌性病毒的保护作用。

Antiinflammatory drugs: protection of a bacterial virus as an in vitro biological measure of free radical activity.

作者信息

Hiller K O, Hodd P L, Willson R L

出版信息

Chem Biol Interact. 1983 Dec;47(3):293-305. doi: 10.1016/0009-2797(83)90165-5.

DOI:10.1016/0009-2797(83)90165-5
PMID:6317211
Abstract

The effects of the hydroxyl free radical (OH), the superoxide free radical (O2-) and the trichloromethyl peroxy free radical (CC13O2) on the survival of bacteriophage T2 have been studied in the absence and presence of several non-steroidal anti-inflammatory drugs (NSAID). The trichloromethylperoxy radical derived from carbon tetrachloride is considerably more effective than the hydroxyl radical in inactivating the virus: the superoxide radical has only a minor inactivating effect. All the NSAID investigated (flurbiprofen, ibuprofen, sulindac, piroxicam, benoxaprofen, mefenamic acid, diflunisal, aspirin, D-penicillamine, indomethacin and metiazinic acid) inhibit inactivation by OH. This is in agreement with the high rate constants of reaction with this radical determined using the fast reaction technique of pulse radiolysis, i.e. (k greater than 10(9) M-1 S-1). The sulphur-containing drugs, metiazinic acid, piroxicam, penicillamine and sulindac as well as the indole derivative indomethacin, protect the virus from inactivation by the model peroxy radical CC13O2 (the dose modifying factor, DMF greater than 20). In contrast, acetylsalicylic acid related drugs, such as diflunisal, the anthranilic acid derivative, mefenamic acid, and some phenylpropionic acid derivatives, such as flurbiprofen, exhibit only a very small or no protective effect (DMF less than 2). As with OH, the ability of the drugs to protect the virus from inactivation by the peroxy radical is in agreement with their corresponding rate constants of reaction determined by pulse radiolysis.

摘要

在有无几种非甾体抗炎药(NSAID)存在的情况下,研究了羟基自由基(OH)、超氧阴离子自由基(O2-)和三氯甲基过氧自由基(CC13O2)对噬菌体T2存活的影响。由四氯化碳衍生的三氯甲基过氧自由基在使病毒失活方面比羟基自由基有效得多:超氧阴离子自由基只有轻微的失活作用。所研究的所有NSAID(氟比洛芬、布洛芬、舒林酸、吡罗昔康、苯恶洛芬、甲芬那酸、二氟尼柳、阿司匹林、D-青霉胺、吲哚美辛和甲氮嗪酸)均抑制OH引起的失活。这与使用脉冲辐射分解的快速反应技术测定的与该自由基反应的高速率常数一致,即(k大于10(9) M-1 S-1)。含硫药物、甲氮嗪酸、吡罗昔康、青霉胺和舒林酸以及吲哚衍生物吲哚美辛可保护病毒免受模型过氧自由基CC13O2的失活作用(剂量修正因子,DMF大于20)。相比之下,乙酰水杨酸相关药物,如二氟尼柳、邻氨基苯甲酸衍生物甲芬那酸,以及一些苯丙酸衍生物,如氟比洛芬,仅表现出非常小的保护作用或无保护作用(DMF小于2)。与OH的情况一样,药物保护病毒免受过氧自由基失活的能力与其通过脉冲辐射分解测定的相应的相应反应速率常数一致。

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