Critical redox and allosteric aspects of nitric oxide interactions with hemoglobin.

Critical redox and allosteric aspects of nitric oxide interactions with hemoglobin.
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DOI:
10.1089/ars.2004.6.979
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发表时间:
2004-10
影响因子:
6.6
通讯作者:
C. Bonaventura;A. Fago;R. Henkens;A. L. Crumbliss
C. Bonaventura;A. Fago;R. Henkens;A. L. Crumbliss
中科院分区:
生物学2区
文献类型:
--
作者:
C. Bonaventura;A. Fago;R. Henkens;A. L. Crumbliss

文献摘要

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一氧化氮(NO)是一种重要的信号分子。血红蛋白(Hb)的血红素和巯基上的相对长寿命的NO加合物可以使NO执行长距离信号功能。尽管取得了重大进展,但仍存在尚未解决的问题,关于Hb在调节影响血压调节的NO信号传导事件中的可能作用。在这篇综述中,我们总结了最近的报告有关的氧化还原和变构方面的NO/血红蛋白的相互作用,推进了我们的理解的生理意义的NO结合血红素基团(形成NO-Hb)和反应促进形成S-亚硝化血红蛋白(SNO-Hb)。变构机制通过改变NO-Hb的寿命和SNO-Hb的性质来改变NO/Hb复合物的生物活性。氧化还原反应是重要的,因为NO及其氧化产物可能具有复杂的化学性质。亚铁和铁血红素网站的反应有不同的后果和亲和力与NO的相互作用。此外,在血红素基团的氧化还原变化影响SH基团的反应性,反之亦然。尽管在体内发现低水平的NO-Hb和SNO-Hb,但最近的研究结果并不排除NO-Hb或SNO-Hb参与NO依赖的信号传导反应。
Nitric oxide (NO) is an important signaling molecule. Relatively long-lived NO adducts at the heme and SH groups of hemoglobin (Hb) could enable NO to carry out long-range signaling functions. In spite of significant advances, there remain as yet unresolved issues regarding the possible role of Hb in moderating NO-signaling events that affect blood pressure regulation. In this review, we summarize recent reports concerning the redox and allosteric aspects of NO/Hb interactions that have advanced our understanding of the physiological significance of NO binding to heme groups (forming NO-Hb) and of reactions promoting formation of S-nitrosated Hb (SNO-Hb). Allosteric mechanisms modify the bioactivity of NO/Hb complexes by altering the lifetime of NO-Hb and the properties of SNO-Hb. Redox reactions are significant because of the complex chemistry possible for NO and its oxidation products. Reactions at ferrous and ferric heme sites have differing consequences and affinities for interactions with NO. Moreover, redox changes at heme groups affect reactivity of SH groups and vice versa. In spite of low levels of NO-Hb and SNO-Hb found in vivo, recent findings do not rule out participation of NO-Hb or SNO-Hb in NO-dependent signaling reactions.