Degradation of neurotoxin β-N-methylamino-L-alanine by UV254 activated persulfate: Kinetic model and reaction pathways

Abstract

In this study, the degradation of β-N-methylamino -L-alanine (BMAA; a novel neurotoxin produced by cyanobacteria) in the UV254/persulfate (PS) system was investigated. The degradation of BMAA satisfied the pseudo-first-order kinetic model. Moreover, the effects of reaction parameters (PS concentration, BMAA concentration, and pH) and water matrix (natural organic matter (NOM) and some anions) were evaluated. The second-order rate constants between BMAA and SO4− or OH at pH 7 were 4.75 × 10 9 M −1·s −1 and 5.49 × 10 9 M −1·s −1, respectively, as measured by a competition kinetics experiment. The results of the steady-state kinetics model and scavenging experiments indicated that SO4− was the major radical contributing to BMAA degradation in the UV254/PS system. Moreover, pH significantly affected the degradation rate of BMAA, and the highest rate was obtained at pH 8 with a pseudo-first-order rate constant (kobs) of 1.039 min−1. However, the degradation of BMAA was inhibited in aqueous solution due to the influence of the water matrix. The kobs decreased in the presence of NOM and chloride ions (Cl−) and increased in the presence of bicarbonate (HCO3−). Given that the degradation rate of total organic carbon (TOC) was lower than that of BMAA, the transformation products and a possible degradation pathway were investigated. The C-N bond on BMAA may be attacked by radicals, and BMAA may be transformed into 2,3-diaminopropionic acid or L-alanine. Moreover, BMAA could also be converted to 2-hydroxy-3-methylamino propanoic acid through hydroxylation. Three different BMAA transformants were further oxidized to generate pyruvic acid, after which decarboxylation leads to the formation of acetic acid from pyruvate.