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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Dinitrosyliron complexes and the mechanism(s) of cellular protein nitrosothiol formation from nitric oxide
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Dinitrosyliron complexes and the mechanism(s) of cellular protein nitrosothiol formation from nitric oxide

机译：一氧化二氮铁配合物和一氧化氮形成细胞蛋白亚硝基硫醇的机理

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摘要

Nitrosothiols (RSNO), formed from thiols and metabolites of nitric oxide (·NO), have been implicated in a diverse set of physiological and pathophysiological processes, although the exact mechanisms by which they are formed biologically are unknown. Several candidate nitrosative pathways involve the reaction of ·NO with O_2, reactive oxygen species (ROS), and transition metals. We developed a strategy using extracellular ferrocyanide to determine that under our conditions intracellular protein RSNO formation occurs from reaction of ·NO inside the cell, as opposed to cellular entry of nitrosative reactants from the extracellular compartment. Using this method we found that in RAW 264.7 cells RSNO formation occurs only at very low (< 8 μM) O_2 concentrations and exhibits zero-order dependence on ·NO concentration. Indeed, RSNO formation is not inhibited even at O_2 levels < 1 μM. Additionally, chelation of intracellular chelatable iron pool (CIP) reduces RSNO formation by > 50%. One possible metal-dependent, O_2-independent nitrosative pathway is the reaction of thiols with dinitrosyliron complexes (DNIC), which are formed in cells from the reaction of ·NO with the CIP. Under our conditions, DNIC formation, like RSNO formation, is inhibited by ≈50% after chelation of labile iron. Both DNIC and RSNO are also increased during overproduction of ROS by the redox cycler 5,8-dimethoxy-1,4-naphtho-quinone. Taken together, these data strongly suggest that cellular RSNO are formed from free ·NO via transnitrosation from DNIC derived from the CIP. We have examined in detail the kinetics and mechanism of RSNO formation inside cells.
机译：由硫醇和一氧化氮代谢物（·NO）形成的亚硝基硫醇（RSNO）与多种生理和病理生理过程有关，尽管它们在生物学上形成的确切机理尚不清楚。亚硝化的几种途径涉及·NO与O_2，活性氧（ROS）和过渡金属的反应。我们开发了一种使用细胞外亚铁氰化物的策略，以确定在我们的条件下，细胞内蛋白质RSNO的形成是由细胞内·NO的反应引起的，这与亚硝化反应物从细胞外腔进入细胞的过程相反。使用这种方法，我们发现在RAW 264.7细胞中，RSNO的形成仅在非常低（<8μM）的O_2浓度下发生，并且对NO浓度呈零级依赖性。实际上，即使在O_2水平<1μM时，也不会抑制RSNO的形成。此外，细胞内可螯合铁池（CIP）的螯合使RSNO的形成减少了50％以上。一种可能的依赖金属，不依赖O_2的亚硝化途径是硫醇与二亚硝基铁络合物（DNIC）的反应，后者是由·NO与CIP反应形成的。在我们的条件下，不稳定铁螯合后，DNIC的形成（如RSNO的形成）被抑制了约50％。在氧化还原循环剂5,8-二甲氧基-1,4-萘醌的过量生产ROS过程中，DNIC和RSNO都增加。综上所述，这些数据强烈表明，细胞的RSNO是由来自CIP的DNIC通过反硝化作用由游离·NO形成的。我们已经详细研究了细胞内RSNO形成的动力学和机理。

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    Charles A. Bosworth; Charles A. Bosworth Jr.; Jaroslaw W. Zmijewski; Qian Li; Jack R. Lancaster;

  • 作者单位

    Departments of Physiology and Biophysics, University of Alabama, Birmingham, AL 35205 Departments of Center for Free Radical Biology, University of Alabama, Birmingham, AL 35205;

    Centro de Ciencias Naturais e Humanas, Universidade Federal do ABC, CEP 09210-170, Santo Andre, Sao Paulo, Brazil;

    Departments of Center for Free Radical Biology, University of Alabama, Birmingham, AL 35205 Departments of Medicine, University of Alabama, Birmingham, AL 35205;

    Departments of Center for Free Radical Biology, University of Alabama, Birmingham, AL 35205 Departments of Anesthesiology, University of Alabama, Birmingham, AL 35205;

    Departments of Physiology and Biophysics, University of Alabama, Birmingham, AL 35205 Departments of Center for Free Radical Biology, University of Alabama, Birmingham, AL 35205 Departments of Anesthesiology, University of Alabama, Birmingham, AL 35205 Departments of Environmental Health Sciences,University of Alabama, Birmingham, AL 35205;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    iron; nitrosation; reactive nitrogen species; reactive oxygen species; chelatable iron;

    机译：铁;亚硝化活性氮活性氧螯合铁;

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