Evaluating Diazene to N₂ Interconversion at Iron-Sulfur Complexes

Biological N-2 reduction occurs at sulfur-rich multiiron sites, and an interesting potential pathway is concerted double reduction/ protonation of bridging N-2 through PCET. Here, we test the feasibility of using synthetic sulfur-supported diiron complexes to mimic this pathway. Oxidative proton transfer from mu-eta(1) : eta(1)-diazene (HN=NH) is the microscopic reverse of the proposed N-2 fixation pathway, revealing the energetics of the process. Previously, Sellmann assigned the purple metastable product from two-electron oxidation of [{Fe2+(PPr3)L-1}(2)(mu-eta(1) : eta(1)-N2H2)] (L-1=tetradentate SSSS ligand) at -78 degrees C as [{Fe2+(PPr3)L-1}(2)(mu-eta(1) : eta(1)-N-2)](2+), which would come from double PCET from diazene to sulfur atoms of the supporting ligands. Using resonance Raman, M & ouml;ssbauer, NMR, and EPR spectroscopies in conjunction with DFT calculations, we show that the product is not an N-2 complex. Instead, the data are most consistent with the spectroscopically observed species being the mononuclear iron(III) diazene complex [{Fe(PPr3)L-1}(eta(2)-N2H2)](+). Calculations indicate that the proposed double PCET has a barrier that is too high for proton transfer at the reaction temperature. Also, PCET from the bridging diazene is highly exergonic as a result of the high Fe3+/2+ redox potential, indicating that the reverse N-2 protonation would be too endergonic to proceed. This system establishes the "ground rules" for designing reversible N-2/N2H2 interconversion through PCET, such as tuning the redox potentials of the metal sites.