Atrazine residue in the environment continues to threaten aquatic ecosystem and human health owing to its adverse effect. However, limited researches focused on degradation mechanism of atrazine by UV/bisulfite, especially risk of intermediates at cellular and molecular level has not been seriously elaborated. In current work, transformation patterns and residual toxicity of intermediates of atrazine by UV/bisulfite were systematically investigated. The atrazine degradation was described by a pseudo first-order kinetic model (Kobs = 0.1053 min-1). The presence of H2PO4-, HCO3- and HA had a powerful inhibition. Scavenging test of radicals illustrated that SO4•-, •OH and O2•- existed in UV/bisulfite system, SO4•- and •OH were mainly responsible for atrazine degradation. Eight degradation intermediates were identified, which were involved in dealkylation, alkyl oxidation, dechlorination-hydroxylation, and alkylic-hydroxylation. E. coli as a model microorganism was selected to assess the risk of degradation intermediates. The levels of reactive oxygen species, MDA and Na+/K+-ATPase were declined, suggesting that oxidative damage induced by these intermediates was weakened. According to differential metabolites expression analysis, several key metabolites including aspartate, L-tryptophan, L-asparagine, cytidine, cytosin, stearic acid, behenic acid, were up-regulated, and glutathione, cadaverin, L-2-hydroxyglutaric acid and phytosphingosine were downregulated, clarifying that effective detoxification of atrazine can be performed by UV/bisulfite.
Keywords: Atrazine; Bisulfite; Differential metabolites expression; Intermediates products; Sulfate radical.
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