No abstract

At ambient temperatures, neutral pH and ultralow concentrations (low nM), the bis(sulfonamido)bis(amido) oxidation catalyst [Fe{4-NO 2 C 6 H 3 -1,2-(NCOCMe 2 NSO 2 ) 2 CHMe}(OH 2 )] − (1) has been shown to catalyze the addition of an oxygen atom to microcystin-LR. This persistent bacterial toxin can contaminate surface waters and render drinking water sources unusable when nutrient concentrations favor cyanobacterial blooms. In mechanistic studies of this oxidation, while the pH was controlled with phosphate buffers, it became apparent that iron ejection from 1 becomes increasingly problematic with increasing [phosphate] (0.3−1.0 M); 1 is not noticeably impacted at low concentrations (0.01 M). At pH < 6.5 and [phosphate] ≥ 1.0 M, 1 decays quickly, losing iron from the macrocycle. Iron ejection is surprisingly mechanistically complex; the pseudo-first-order rate constant k obs has an unusual dependence on the total phosphate concentration ([P t ]), k obs = k 1 [P t ] + k 2 [P t ] 2 , indicating two parallel pathways that are first and second order in [phosphate], respectively. The pH profiles in the 5.5−8.3 range for k 1 and k 2 are different: bellshaped with a maximum of around pH 7 for k 1 and sigmoidal for k 2 with higher values at lower pH. Mechanistic proposals for the k 1 and k 2 pathways are detailed based on both the kinetic data and density functional theory analysis. The major difference between k 1 and k 2 is the involvement of different phosphate species, i.e., HPO 4 2− (k 1 ) and H 2 PO 4 − (k 2 ); HPO 4 2− is less acidic but more nucleophilic, which favors intramolecular rate-limiting Fe−N bond cleavage. Instead, H 2 PO 4 − acts intermolecularly, where the kinetics suggest that [H 4 P 2 O 8 ] 2− drives degradation.