Role of Ligand to Control the Mechanism of Nitric Oxide Reduction of Copper(II) Complexes and Ligand Nitrosation

The nitric oxide reactivity of two copper­(II) complexes, 1 and 2 with ligands L1 and L2, respectively,
[L1 = 5,5,7,12,12,14-hexamethyl-1,4,8,11-tetraazacyclotetradecane, L2 = 5,5,7-trimethyl-[1,4]-diazepane]
have been studied. The copper­(II) center in complex 1 was found to be unreactive toward nitric oxide in pure acetonitrile; however, it displayed reduction in methanol solvent in presence
of base. The copper(II) center in 2, in acetonitrile solvent, on exposure
to nitric oxide has been found to be reduced to copper­(I). The same
reduction was observed in methanol, also, in case of complex 2. In case of complex 1, presumably, the attack
of nitric oxide on the deprotonated amine is the first step, followed
by electron transfer to the copper­(II) center to afford the reduction.
Alternatively, first NO coordination to the Cu­(II) followed by NO+ migration to the secondary amine is the most probable in
case of complex 2. The observation of the transient intermediate
in UV–visible and FT-IR spectroscopy prior to reduction in
case of complex 2 also supports this possibility. In both cases,
the reduction resulted into N-nitrosation; in 1, only
mononitrosation was observed whereas complex 2 afforded
dinitrosation as major product along with a minor amount of mononitrosation.
Thus, it is evident from the present study that the macrocyclic ligands
prefer the deprotonation pathway leading to mononitrosation; whereas
nonmacrocyclic ones prefer the [CuII–NO] intermediate
pathway resulting into nitrosation at all the available sites of the
ligand as major product.