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

Abstract

Dinitrosyliron complexes (DNICs) are organometallic-like compounds of biological significant in that they appear in vivo as products of NO degradation of iron-sulfur culters; 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) not: 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 cycteine and glutathione themselves are subject to thiolate-disulfide redox processes, which when coupled to DNICs may lead to intricate redoc processes involving iron, NO, and RS-/RS center dot. Making use of an N-heterocyclic carbene-stabilized DNIC, (NHC)(RS)Fe(NO)(2), we have explored the DNIC-promoted RS-/RS center dot 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 center dot ligand substitution. Kinetic studies indicate a bimolecular process, rate = k [Fe(NO)(2)](1)[CO](1), and activation parameters derived for k(obs) dependence on temperature similarly indicate an associative mechanism. This mechanism is further defined by density functional theory computaitons. Computational results indicate a unique role for the delocalized frontier molecular orbitals of the Fe(NO)(2) unit, permitting ligand exchange of RS center dot and CO through an initial side-on approach of CO to the electron-rich N-Fe-N site, ultimately resulting in 5-coordinate, 19-electron intermeidate with elogated Fe-SR bond and with the NO ligands accommodating the excess charge.