NO Reduction to N2O Triggered by a Dinuclear Dinitrosyl Iron Complex via the Associated Pathways of Hyponitrite Formation and NO Disproportionation.

In spite of the comprehensive study of the metal-mediated conversion of NO to N2O disclosing the conceivable processes/mechanism in biological and biomimetic studies, in this study, the synthesis cycles and mechanism of NO reduction to N2O triggered by the electronically localized dinuclear {Fe(NO)2}10-{Fe(NO)2}9 dinitrosyl iron complex (DNIC) [Fe(NO)2(µ-bdmap)Fe(NO)2(THF)] (1) (bdmap = 1,3- bis(dimethylamino)-2-propanolate) were investigated in detail. Reductive conversion of NO to N2O triggered by complex 1 in the presence of exogenous ·NO occurs via the simultaneous formation of hyponitrite-bound {[Fe2(NO)4(µ-bdmap)]2(κ4-N2O2)} (2) and [NO2]--bridged [Fe2(NO)4(µ-bdmap)(µ-NO2)] (3) (NO disproportionation yielding N2O and complex 3). EPR/IR spectra, single-crystal X-ray diffraction, and the electrochemical study uncover the reversible redox transformation of {Fe(NO)2}9-{Fe(NO)2}9 [Fe2(NO)4(µ-bdmap)(µ-OC4H8)]+ (7) ↔ {Fe(NO)2}10-{Fe(NO)2}9 1 ↔ {Fe(NO)2}10-{Fe(NO)2}10 [Fe(NO)2(µ-bdmap)Fe(NO)2]- (6) and characterize the formation of complex 1. Also, the synthesis study and DFT computation feature the detailed mechanism of electronically localized {Fe(NO)2}10-{Fe(NO)2}9 DNIC 1 reducing NO to N2O via the associated hyponitrite-formation and NO-disproportionation pathways. Presumably, the THF-bound {Fe(NO)2}9 unit of electronically localized {Fe(NO)2}10-{Fe(NO)2}9 complex 1 served as an electron buffering reservoir for accommodating electron redistribution, and the {Fe(NO)2}10 unit of complex 1 acted as an electron-transfer channel to drive exogeneous ·NO coordination to yield proposed relay intermediate κ2-N,O-[NO]--bridged [Fe2(NO)4(µ-bdmap)(µ-NO)] (A) for NO reduction to N2O.

NO-to-[N2O2]2--to-N2O Conversion Triggered by {Fe(NO)2}10-{Fe(NO)2}9 Dinuclear Dinitrosyl Iron Complex.

Flavodiiron nitric oxide reductases (FNORs) evolved in some pathogens are known to detoxify NO via two-electron reduction to N2O to mitigate nitrosative stress. In this study, we describe how the electronically localized {Fe(NO)2}10-{Fe(NO)2}9 dinuclear dinitrosyl iron complex (dinuclear DNIC) [(NO)2Fe(µ-bdmap)Fe(NO)2(THF)] (2) (bdmap = 1,3-bis(dimethylamino)-2-propanolate) can induce a reductive coupling of NO to form hyponitrite-coordinated tetranuclear DNIC, which then converts to N2O. Upon the addition of 1 equiv of NO into the dinuclear {Fe(NO)2}10-{Fe(NO)2}9 DNIC 2, the proposed side-on-bound [NO]--bridged [(NO)2Fe(µ-bdmap)(κ2-NO) Fe(NO)2] intermediate may facilitate intermolecular (O)N-N(O) bond coupling to yield the paramagnetic tetranuclear quadridentate trans-hyponitrite-bound {[(NO)2Fe(µ-bdmap)Fe(NO)2]2(κ4-N2O2)} that transforms to [Fe(NO)2(µ-bdmap)]2, along with the release of N2O upon Hbdmap (1,3-bis(dimethylamino)-2-propanol) added.