On TAML Catalyst Resting State Lifetimes: Kinetic, Mechanistic, and Theoretical Insight into Phosphate-Induced...

At ambient temperatures, neutral pH and ultralow concentrations (low nM), the bis(sulfonamido)bis(amido) oxidation catalyst [Fe{4-NO₂C₆H₃-1,2-(NCOCMe₂NSO₂)₂CHMe}(OH₂)]^- (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 = k₁[P_t] + k₂[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 k₁ and k₂ are different: bell-shaped with a maximum of around pH 7 for k₁ and sigmoidal for k₂ with higher values at lower pH. Mechanistic proposals for the k₁ and k₂ pathways are detailed based on both the kinetic data and density functional theory analysis. The major difference between k₁ and k₂ is the involvement of different phosphate species, i.e., HPO₄^2- (k₁) and H₂PO₄^- (k₂); HPO₄^2- is less acidic but more nucleophilic, which favors intramolecular rate-limiting Fe-N bond cleavage. Instead, H₂PO₄^- acts intermolecularly, where the kinetics suggest that [H₄P₂O₈]^2- drives degradation.