Abstract
The formation mechanisms of DNIC produced by nitosylation of the biomimetic ferredoxin [Fe4S4(SR)4]2- and [4Fe-4S] cluster precursor[Fe4(SR)10]2– (R = Et, Ph) was exhibited. After isolating [Fe4S3(NO)7]– (2) from nitosylation of [Fe4S4(SR)4]2-, the dinitrosyl or mononitrosyl iron cores of complex 2 degraded to DNICs [(RS)2Fe(NO)2]– (5) or reduced to [Fe4S3(NO)7]2– via nucleophilic attack of [SR]– (R = Ph, Et), respectively. Complexes [Fe4S4(NO)4]– (3) (g = 1.624 at 4 K) and [Fe4S3(NO)7]2– (g = 2.020 at 250 K), intermediate and byproduct of [Fe4S4(SR)4]2- degradation, suggested the variety of EPR spectra for modification of [4Fe-4S] clusters with NO in biological system. Nitrosylation of the [4Fe-4S] cluster precursors [Fe4(SR)10]2- (R = SPh, SEt) led to the formation of the MNICs [(RS)3Fe(NO)]– (7), then DNICs [(RS)2Fe(NO)2]– (5) and RRE [Fe(μ-SR)(NO)2]2 (8) were also demonstrated in further nitrosylation. Interestingly, reaction of [Fe4(SPh)10]2– and [NO2]– only resulted in the formation of [(PhS)3Fe(NO)]– (7-Ph). In this work, anionic RRE syn/anti-[Fe(μ-SEt)(NO)2]2– (9) and [Fe(μ-SEt)(NO)2]2 (8-Et) was synthesized, and the oxidation state of iron cores were about +0.87 and +1.0, respectively, characterized by X-ray Fe K-edge and L-edge absorption spectra. The different nucleophile ([SEt]– vs [(EtS)2Fe(NO)2]– vs [(PhS)2Fe(NO)2]–) functions to control the reaction pathways (bridged-thiolate cleavage vs reduction vs no reaction) upon reaction of [Fe(μ-SR)(NO)2]2 (8) and nucleophiles. It was confirmed [(EtS)2Fe(NO)2]– (5-Et) and [Fe(μ-SEt)(NO)2]2– (9) can be oxidized to form complex 8 by NO, and supported the probable factor that [Fe(μ-SR)(NO)2]2 was major product in the nitrosylation of FNR. Importantely, [Fe(μ-SEt)(NO)2]2– (9) and d9-DNIC (proposed reduced form of [(RS)2Fe(NO)2]–) have very similar synthetic method and EPR spectra.