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

Abstract

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.