期刊
NATURE CHEMICAL BIOLOGY
卷 11, 期 7, 页码 504-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/NCHEMBIO.1814
关键词
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资金
- US National Institutes of Health [R01-HL058115, R01-HL64937, P01-HL103455, R01-AT006822]
- AHA [14GRNT20170024]
The current perspective holds that the generation of secondary signaling mediators from nitrite (NO2-) requires acidification to nitrous acid (HNO2) or metal catalysis. Herein, the use of stable isotope-labeled NO2- and LC-MS/MS analysis of products reveals that NO2- also participates in fatty acid nitration and thiol S-nitrosation at neutral pH. These reactions occur in the absence of metal centers and are stimulated by autoxidation of nitric oxide ((NO)-N-center dot) via the formation of symmetrical dinitrogen trioxide (nitrous anhydride, symN(2)O(3)). Although theoretical models have predicted physiological symN(2)O(3) formation, its generation is now demonstrated in aqueous reaction systems, cell models and in vivo, with the concerted reactions of (NO)-N-center dot and NO2- shown to be critical for symN(2)O(3) formation. These results reveal new mechanisms underlying the NO2- propagation of (NO)-N-center dot signaling and the regulation of both biomolecule function and signaling network activity via NO2--dependent nitrosation and nitration reactions.
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