Fe(V) Dominates the Toxicity Increase Pathway during Ferrate(VI) Degradation of Fluoroquinolone Antibiotics

Environmental accumulation of fluoroquinolones (FQs) has brought concerns over their potential risks to human health. This study found that ferrate (Fe(VI)) could efficiently degrade norfloxacin (NOR), ciprofloxacin (CIP), and levofloxacin (LEV). However, cytotoxicity to mammalian cells of NOR, CIP, and LEV dramatically increased from 9.41, 8.34, and 11.05 mg phenol/L to 20.76, 26.13, and 32.45 mg phenol/L after reacting with Fe(VI) for 3 min. Intracellular oxidative stress in the mammalian cells also increased, suggesting the risk of applying Fe(VI) for FQ degradation. Fe(V) was demonstrated to play the major role in FQ degradation by kinetics investigation, probe contaminant (PMSO and 2,2 '-azino-bis-(3-ethylbenzothiazoline-6-sulfonate) (ABTS)), and pyrophosphate competing experiments. Density functional theory (DFT) calculation and toxicity prediction suggested that, in the CIP-ferrate system, Fe(V) increased the toxicity via oxidizing the piperazine group to -NH2. In the NOR-ferrate and LEV-ferrate systems, Fe(V) mainly attacked the quinolone ring. The unstable products underwent subsequent carboxylation or hydroxylation, leading to the further increased toxicity. The current research on micropollutant removal focused on applying various approaches to activate ferrate to generate high-valent iron intermediates with stronger oxidizing capacity. Our study gave a risk warning that high-valent iron intermediates might play an important role in increasing the toxicity of micropollutants.

Automated summary

This study found that ferrate could efficiently degrade fluoroquinolones, but their cytotoxicity to mammalian cells dramatically increased after reacting with ferrate. The research also revealed the important role of high-valent iron intermediates in the degradation of micropollutants.