Dinitrosyliron complexes (DNICs) are biologically relevant molecules involved in nitric oxide (NO) transport and storage in biological systems. Biological DNICs are known to be products of iron-sulfur cluster degradation by excess NO, or derived from the chelatable iron pool (CIP) in cells; synthetic DNIC analogs have potential as NO storage and release agents with therapeutic benefit. The dinitrosyl iron unit is known to exist in two redox levels; its oxidized and reduced forms, {Fe(NO)2}9 and {Fe(NO)2}10 respectively (Enemark-Feltham notation) with redox potentials dependent on ancillary ligands. Previous work determined that oxidized {Fe(NO)2}9 could be reduced to {Fe(NO)2}10 through carbon monoxide (CO)/RS� ligand substitution, utilizing an N-heterocyclic carbene (NHC) to stabilize the DNIC. Kinetic and computational results suggested the reaction follows an associative mechanism initiated by the delocalized Fe(NO)2 frontier orbitals, followed by the formation of a 19 electron intermediate. To provide further evidence for the proposed mechanism, (NHC)(SPhX)Fe(NO)2 derivatives were synthesized with varying para-substituents on the phenyl thiolate. The series included p-OCH3, p-CH3, p-Cl, p-CF3, and p-NO2 derivatives, which were characterized by means of X-ray crystallography and IR spectroscopy. Kinetic studies were also carried out using in situ IR spectroscopy, and a Hammett Analysis was conducted to monitor the electron density of the N-Fe-N unit. The rate data thus obtained is in accordance with the computationally purposed mechanism showing reaction rates accelerated by electron donating substituents, and slowed by electron withdrawing substituents.

Further mechanistic studies of carbon monoxide induced reductive elimination of disulfide in N-heterocyclic carbene (NHC)/thiolate dinitrosyl iron complexes (DNICs)

247th National Meeting (2014)

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