Mechanistic study on thiacloprid transformation: Free radical reactions

- OH/eaq− exhibits appreciable reactivity towards the insecticide thiacloprid.
- The majority of OH attack the key cyanoiminothiazolidine pharmacophore.
- α-aminoalkyl, N-centred, α-(alkylthio)alkyl and >S-OH radicals form on this moiety.
- One-electron reduction occurs at the pyridyl function yielding pyridinyl radicals.
- Destruction of pharmacologically important substructures is anticipated.

Free radical induced oxidation/reduction mechanisms of the hazardous water contaminant thiacloprid have been unravelled using pulse radiolysis techniques involving transient spectral analysis and redox titration experiments. The OH-induced oxidation of thiacloprid proceeds with appreciable rate, the reaction rate constant has been determined to be kOH = 4.8 × 109 mol−1 L s−1. The OH attack leaves behind a rather complex free radical system consisting of ∼9% α-aminoalkyl radicals, ∼31% aminyl + aminium nitrogen centred radicals, ∼46% radicals at the sulfur and ∼14% hydroxycyclohexadienyl radical of the pyridyl moiety. Since ∼86% of radicals are formed on the key cyanoiminothiazolidine pharmacophore, OH is anticipated to be an appropriate candidate for inactivation of this biologically active pollutant. The one-electron reduction exerted by eaq− occurs at a diffusion controlled rate. As a result of the eaq− attack pyridinyl radical forms that takes part in subsequent protonation and dechlorination processes. The course of events is anticipated to lead to the destruction of another important part of the molecule in respect to insecticidal activity.

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