Carbon Monoxide Induced Reductive Elimination of Disulfide in an N‑Heterocyclic Carbene (NHC)/ Thiolate Dinitrosyl Iron Complex (DNIC)

Dinitrosyliron complexes (DNICs) are organometallic-like compounds of biological significance in that they appear <i>in vivo</i> as products of NO degradation of iron–sulfur clusters; synthetic analogues have potential as NO storage and releasing agents. Their reactivity is expected to depend on ancillary ligands and the redox level of the distinctive Fe­(NO)₂ unit: paramagnetic {Fe­(NO)₂}⁹, diamagnetic dimerized forms of {Fe­(NO)₂}⁹ and diamagnetic {Fe­(NO)₂}¹⁰ DNICs (Enemark–Feltham notation). The typical biological ligands cysteine and glutathione themselves are subject to thiolate-disulfide redox processes, which when coupled to DNICs may lead to intricate redox processes involving iron, NO, and RS^–/RS•. Making use of an N-heterocyclic carbene-stabilized DNIC, (NHC)­(RS)­Fe­(NO)₂, we have explored the DNIC-promoted RS^–/RS• oxidation in the presence of added CO wherein oxidized {Fe­(NO)₂}⁹ is reduced to {Fe­(NO)₂}¹⁰ through carbon monoxide (CO)/RS• ligand substitution. Kinetic studies indicate a bimolecular process, rate = <i>k</i> [Fe­(NO)₂]¹[CO]¹, and activation parameters derived from <i>k</i>_obs dependence on temperature similarly indicate an associative mechanism. This mechanism is further defined by density functional theory computations. Computational results indicate a unique role for the delocalized frontier molecular orbitals of the Fe­(NO)₂ unit, permitting ligand exchange of RS• and CO through an initial side-on approach of CO to the electron-rich N–Fe–N site, ultimately resulting in a 5-coordinate, 19-electron intermediate with elongated Fe–SR bond and with the NO ligands accommodating the excess charge