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首页> 外文期刊>Journal of biochemical and molecular toxicology >Lidocaine: an inhibitor in the free-radical-induced hemolysis of erythrocytes.
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Lidocaine: an inhibitor in the free-radical-induced hemolysis of erythrocytes.

机译：利多卡因：自由基诱导的红细胞溶血的抑制剂。

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摘要

Lidocaine was reported to protect erythrocytes from hemolysis induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). Since AAPH-induced hemolysis was a convenient in vitro experimental system to mimic erythrocytes undergoing peroxyl radicals attack, the aim of this work was to investigate the antioxidant effect of lidocaine on AAPH-induced hemolysis by chemical kinetics. As a result, one molecule of lidocaine can only trap 0.37 radical, much lower than melatonin. Meanwhile, lidocaine cannot protect erythrocytes from hemolysis induced by hemin, which the mechanism of hemolysis was due to the erythrocyte membrane destroyed by hemin. Accordingly, lidocaine protected erythrocytes by scavenging radicals preferentially rather than by stabilizing membrane. Moreover, the interactions of lidocaine with two radical species, including 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonate) radical cation (ABTS(+*)) and 2,2'-diphenyl-1-picrylhydrazyl (DPPH), indicated that lidocaine can reduce ABTS(+*) with 260 microM as the 50% inhibition concentration (IC(50)) and cannot react with DPPH. Thus, lidocaine served as a reductant rather than a hydrogen donor to interact with radicals. Finally, the quantum calculation proved that, compared with the melatonin radical, the stabilization of N-centered radical of lidocaine was higher than the amide-type N-centered radical but lower than the indole-type N-centered radical in melatonin. These results provided basic information for lidocaine to be an antiradical drug.
机译：据报道，利多卡因可以保护红细胞免受2,2'-偶氮双（2-ami基丙烷）二盐酸盐（AAPH）诱导的溶血。由于AAPH诱导的溶血是模拟经历过氧自由基攻击的红细胞的便捷体外实验系统，因此本研究的目的是通过化学动力学研究利多卡因对AAPH诱导的溶血的抗氧化作用。结果，一个利多卡因分子只能捕获0.37个自由基，远低于褪黑激素。同时，利多卡因不能保护红细胞免受血红素引起的溶血，溶血的机制是由于血红素破坏了红细胞膜。因此，利多卡因通过优先清除自由基而不是通过稳定膜来保护红细胞。此外，利多卡因与两个自由基种类的相互作用，包括2,2'-叠氮基双（3-乙基苯并噻唑啉-6-磺酸盐）自由基阳离子（ABTS（+ *））和2,2'-二苯基-1-吡啶并肼基（DPPH） ，表明利多卡因可以以260 microM作为50％抑制浓度（IC（50））降低ABTS（+ *），并且不能与DPPH反应。因此，利多卡因用作还原剂而不是氢供体与自由基相互作用。最后，量子计算证明，与褪黑素自由基相比，利多卡因的N-中心自由基的稳定性高于褪黑激素中酰胺型N-中心自由基，但低于吲哚型N-中心自由基。这些结果为利多卡因是一种抗自由基药物提供了基本信息。

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