Triggering N(2) uptake via redox-induced expulsion of coordinated NH(3) and N(2) silylation at trigonal bipyramidal iron.

The biological reduction of N(2) to give NH(3) may occur by one of two predominant pathways in which nitrogenous N(x)H(y) intermediates, including hydrazine (N(2)H(4)), diazene (N(2)H(2)), nitride (N(3-)) and imide (NH(2-)), may be involved. To test the validity of hypotheses on iron's direct role in the stepwise reduction of N(2), model systems for iron are needed. Such systems can test the chemical compatibility of iron with various proposed N(x)H(y) intermediates and the reactivity patterns of such species. Here we describe a trigonal bipyramidal Si(o-C(6)H(4)PR(2))(3)Fe-L scaffold (R = Ph or i-Pr) in which the apical site is occupied by nitrogenous ligands such as N(2), N(2)H(4), NH(3) and N(2)R. The system accommodates terminally bound N(2) in the three formal oxidation states (iron(0), +1 and +2). N(2) uptake is demonstrated by the displacement of its reduction partners NH(3) and N(2)H(4), and N(2) functionalizaton is illustrated by electrophilic silylation.