Gas-phase ion chemistry of the pesticide imidacloprid: Proton driven radical fragmentation of the nitro-guanidine functional group

Electrospray ionization (ESI) coupled with low-energy collision-induced dissociation (CID) was used to establish the role of the charge in the fragmentation reactions of the [M+H](+), [M+CH3](+) (a methylated fixed charge derivative), [M-H](-) and [M+Li](+) of imidacloprid, 1, which contains both a nitroguanidine functional group, a known 'explosophore', and a remote chloropyridine group. The major primary fragmentation pathways involve fragmentation of the nitroguanidine functional group in all cases, although the type of neutrals lost varies. Bond homolysis via NO2 center dot loss is a major fragmentation pathway for [M+H](+) (similar to 55% relative abundance), but is virtually absent for [M+CH3] (in which the charge is located on the pyridine nitrogen and is remote from the nitroguanidine group), [M-H](-) and [M+Li](+) (<1% relative abundance), indicating the NO2 center dot loss from [M+H](+) occurs via a mechanism in which the proton is localized at the nitroguanidine functional group. DFT calculations indicate that the favorable site of protonation in imidacloprid is at the pyridine nitrogen by over 24 kJ/mol in both the gas and solution phases, and that the barrier to proton transfer to the imine nitrogen is energetically accessible under conditions of CID. In addition, the favored protonation site switches from the pyridine group of protonated imidacloprid to the guanidinyl group upon loss of NO2 center dot, corresponding to a reversal in the favorable protonation site of over 50 kJ/mol. These results all suggest that the radical fragmentation of the nitroguanidine explosophore is driven by the proton, which is transferred from the pyridine nitrogen to the nitroguanidine group upon CID, and the large proton affinity shift for the nitroguanidine group upon loss of NO2 center dot. Crown Copyright (c) 2012 Published by Elsevier B.V. All rights reserved.