Electrocatalytic dihydrogen evolution mechanism of [Fe-2(CO)(4)(kappa(2)-Ph2PCH2CH2PPh2)(mu-S(CH2)(3)S)] and related models of the [FeFe]-hydrogenases active site: a DFT investigation

A DFT study of protonation thermodynamics in H-2-evolving biomimetic catalysts related to [FeFe]-hydrogenases active site is presented here. Taking as a reference system the electrocatalytic dihydrogen evolution mechanism recently proposed for the synthetic assembly [Fe-2(CO)(4)(kappa(2)-Ph2PCH2CH2PPh2)(mu-S(CH2)(3)S)] (a, which is able to release H-2 after having undergone monoelectron reduction steps and three sequential protonation reactions), we show how the reduction of model complexes to oxidation states lower than those observed in [FeFe]-hydrogenases cofactor leads to a protonation regiochemistry that has no counterpart in the enzymatic mechanism of H-2 production. In particular, double protonation of the metal centers turned out to be disfavored in a by up to 12.5 kcal mol(-1) with respect to alternative protonation paths; as for the regiochemistry of triple protonation, the formation of eta(2)-H-2 adducts is disfavored by at least similar to 25 kcal mol(-1). Structural analysis of the theoretical models also revealed that over-reduction of synthetic complexes, though necessary for observing H-2 evolution from the currently available biomimetic electrocatalysts, can generally impair their structural integrity. Possible approaches for the modulation of protonation regiochemistry are then proposed; in particular, it turned out that a targeted use of sigma-donating ligands showing low basicity can favor double protonation of iron centers