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Issue 6, 2014
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Coordination-triggered NO release from a dinitrosyl iron complex leads to anti-inflammatory activity

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Abstract

Dinitrosyl iron complexes (DNICs) are widely considered NO storage and donor molecules in cells. However, what induces an NO release from iron in DNICs and the subsequent biological consequences remain elusive. The chemistry and biology of the NO release activity of DNICs are reported here. Changes in redox status or coordination number of discrete N-bound DNICs, respectively [Fe(TMEDA)(NO)2] (1) and [Fe(TMEDA)(NO)2I] (2), can generate a metastable {Fe(NO)2}9 DNIC, [Fe(TMEDA)(NO)2]+, with νNO at 1769 and 1835 cm−1 and an EPR signal at g = 2.04, that spontaneously releases NO in solution. The NO release activity of 2 results in the up- and downregulation of heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS), respectively, in murine RAW 264.7 macrophages. Furthermore, treatment with 2 leads to downregulation of pro-inflammatory cytokines, TNF-α and IL-6, and upregulation of the anti-inflammatory cytokine, IL-10. Taken together, these results demonstrate that the appropriate control of redox and coordination chemistry of DNICs could enable them to become anti-inflammatory agents, suggesting a potential new role for cellular DNICs.

Graphical abstract: Coordination-triggered NO release from a dinitrosyl iron complex leads to anti-inflammatory activity

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Publication details

The article was received on 03 Dec 2013, accepted on 19 Feb 2014 and first published on 24 Feb 2014


Article type: Edge Article
DOI: 10.1039/C3SC53319K
Citation: Chem. Sci., 2014,5, 2374-2378
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    Coordination-triggered NO release from a dinitrosyl iron complex leads to anti-inflammatory activity

    K. M. Skodje, M. Kwon, S. W. Chung and E. Kim, Chem. Sci., 2014, 5, 2374
    DOI: 10.1039/C3SC53319K

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