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

Abstract

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-6sulfonate) (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 −NH 2 . 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.

How Should We Activate Ferrate(VI)? Fe(IV) and Fe(V) Tell Different Stories about Fluoroquinolone Transformation and Toxicity Changes

“…P1–2 ( m / z = 364.13) was derived from P1–1 after the loss of CH 2 (14 Da loss from 378.14). P1–3 to P1–5 were formed by ring cleavage or oxygen atom addition until the piperazinyl group transformed into −NH 2 (P1–5, m / z = 307.18). , The terminal product in pathway I (P1–6, m / z = 277.08) was generated from the F atom in P1–5 substitution by −OH. , Furthermore, the f – value was markedly high at N17 (0.57) of the piperazine group, which increased the reactivity of N17, facilitating the addition of −OH to the C16 position (C16–N17). There was also a significant increase in the f – values of the atoms of O25 and N17 (0.061) of P1–1, which increased the susceptibility of the piperazine group to be attacked from high-valent iron species.…”