Advanced oxidation processes (AOPs) exhibit significant potential for water disinfection due to their generation of large quantities of highly oxidizing free radicals. However, the neglect of viable but nonculturable (VBNC) cells obscures their true disinfection efficacy and potential environmental health risks. Therefore, the study evaluated the disinfection effectiveness and mechanisms of typical AOPs, including Fe/H 2 O 2 , Fe/persulfate (PS), and O 3 , from the perspective of the production of VBNC bacteria. The results indicate that Fe/PS exhibits the strongest bacterial inactivation rate (99.94%), and the cells lose their ability to reactivate. Fe/H 2 O 2 and O 3 induce more cells to enter the VBNC state compared to Fe/PS. Moreover, different AOPs result in varying levels of free radical production and utilization efficiency, with SO 4 •− and O 3 exhibiting greater selectivity in deactivating bacteria compared to HO • . The inhibition of VBNC bacteria production by Fe/PS treatment may be attributed to the combined action of HO • and SO 4 •− on microorganisms, leading to oxidative stress and metabolic disruption in bacteria through the inhibition of biofilm formation and aminoacyl-tRNA biosynthesis ( p < 0.05), thereby causing direct bacterial death rather than entry into the VBNC state. In contrast, Fe/H 2 O 2 and O 3 result in the upregulation of the metabolism of alanine, aspartate, and glutamate, as well as styrene degradation capacity by the bacteria, leading to the production of more VBNC bacteria. Overall, the study offers insights into mitigating potential biological risks in water disinfection and developing environmentally friendly and efficient disinfection technologies.
In this work, the presence of ascorbic acid (AsA) in MIL-88B(Fe) / H 2 O 2 system was demonstrated to significantly increase the sulfamethoxazole (SMX) degradation efficiency. The SMX degradation rate in AsA/MIL-88B(Fe) / H 2 O 2 system was 0.177 L/(mg∙min), which was 60 times that of the MIL-88B(Fe) / H 2 O 2 system. Moreover, the study shows that AsA not only promotes SMX degradation in Fenton-like systems but also expands its pH application range. The effect of coexisting anions on the catalytic performance of the AsA/MIL-88B(Fe) / H 2 O 2 system was also investigated. Then, reactive species were detected via quenching experiments, which indicated •OH as the dominant free radical contributing to SMX degradation. Meanwhile, ESR determinations confirmed the existence of •OH and O2 − • in AsA/MIL-88B(Fe) / H 2 O 2 system. The high activity of the AsA/MIL-88B(Fe) / H 2 O 2 system was attributed to the effective surface Fe(III)/Fe(II) cycle promoted by AsA, and a possible mechanism of the AsA/MIL-88B(Fe) / H 2 O 2 system is proposed. The possible pathways for SMX and AsA degradation in the AsA/MIL-88B(Fe) / H 2 O 2 system are proposed based on the identified intermediates and the ecotoxicity analysis was conducted by ECOSAR . Finally, experimental results using the actual surface water and groundwater revealed the excellent availability of AsA/MIL-88B(Fe)/H 2 O 2 system in remediating SMX contaminated water . This study presents a novel, efficient Fenton-like system using AsA and iron-based metal-organic frameworks for sulfonamide removal from water.
Ferroptosis is an iron-dependent programmed cell death modality characterized by the massive accumulation of lipid peroxides (LPO). However, the efficiency of ferroptosis is commonly limited by insufficient supply of iron ions and endogenous hydrogen peroxide (H 2 O 2 ) in the tumor cells. To overcome these drawbacks, MIL-100 NPs were synthesized via a microwave-assisted method to encapsulate β-lapachone (Lap), followed with the hyaluronic acid (HA) surface modification (designated as LMH NPs). LMH NPs exhibited GSH-responsive degradation in the tumor cells to release Lap and Fe 3+ . The released of Lap could generate H 2 O 2 via catalysis by tumor-overexpressed quinone oxidoreductase 1 (NQO1), leading to increased intracellular H 2 O 2 levels. The abundant production of H 2 O 2 could supply substrates for Fe 2+ -mediated Fenton reactions to produce toxic hydroxyl radicals (·OH), thereby promoting LPO accumulation and enhancing ferroptosis. Meanwhile, Fe 3 ⁺ released from LMH NPs was reduced to Fe 2+ through GSH consumption, which could diminish glutathione peroxidase 4 (GPX4) activity. In vitro and in vivo experiments confirmed that LMH NPs possessed effective targeted uptake and exhibited optimal tumor inhibition without significant toxic side effects. Overall, the integrated strategy presents a novel ferroptosis-based clinical approach for enhanced breast cancer therapy. Scheme 1 Preparation process and antitumor mechanisms of LMH NPs. (A) The preparation process of LMH NPs. (B) Antitumor mechanism of LMH NPs through inducing ferroptosis. (C) Lap undergoes a ‘‘futile redox cycling’’ process catalyzed by NQO1. Download: Download high-res image (119KB) Download: Download full-size image
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