| Literature DB >> 35259597 |
Hirotoshi Matsumura1, Abayomi S Faponle2, Peter-Leon Hagedoorn3, Takehiko Tosha4, Sam P de Visser2, Pierre Moënne-Loccoz5.
Abstract
Steady-state kinetics of cytochrome-c dependent denitrifying NO reductases (cNORs) show evidence of substrate inhibition at NO concentrations higher than 10 μM, but the mechanism of inhibition remains unclear. Here, we present low-temperature FTIR photolysis experiments carried out on the NO complex formed by addition of NO to the oxidized cNORs. A differential signal at 1261 cm-1 that downshifts with 15NO and 15N18O is assigned to a ν(NO2) from a bridging diiron-nitrito complex at the heme-nonheme diron site. Theoretical calculations reproduces observed frequencies and isotope shifts. Our experimental results confirm a prior theoretical study by Blomberg and Siegbahn [Blomberg, M. R., and Siegbahn, P. E. M. Biochemistry 2012, 51, 5173-5186] that proposed substrate inhibition through a radical combination reaction between the diferric μ-oxo group and an NO molecule to form a heme Fe(III)-nitrito-FeB(II) inhibitory complex. Stopped-flow experiments suggest that substrate inhibition also occurs after a half-reduction cycle, i.e. when fully-reduced cNOR reduces two NO molecules at the heme-nonheme diferrous active site cluster to produce one N2O molecule and the diferric cluster. These results support catalytic mechanisms that proceed through isomerization of a diferric-hyponitrite transient complex to produce a bridging diferric μ-oxo group and N2O without protonation of the putative hyponitrite intermediate.Entities:
Keywords: Iron proteins; Nitric oxide reductases; Reaction mechanisms; Spectroscopy
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Year: 2022 PMID: 35259597 PMCID: PMC9007887 DOI: 10.1016/j.jinorgbio.2022.111781
Source DB: PubMed Journal: J Inorg Biochem ISSN: 0162-0134 Impact factor: 4.155