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Heterogeneous Fenton reactions of zero-valent iron (ZVI) requires the sufficient release of Fe(II) to catalyze the H 2 O 2 decomposition. However, the rate-limiting step of proton transfer through the passivation layer of ZVI restricted the Fe(II) release via Fe 0 core corrosion. Herein we modified the shell of ZVI with highly proton-conductive FeC 2 O 4 ·2H 2 O by ball-milling (OA-ZVI bm ), and demonstrated its high heterogeneous Fenton performance of thiamphenicol (TAP) removal, with 500 times enhancement of the rate constant. More importantly, the OA-ZVI bm /H 2 O 2 showed little attenuation of the Fenton activity during 13 successive cycles, and was applicable across a wide pH range of 3.5-9.5. Interestingly, the OA-ZVI bm /H 2 O 2 reaction showed pH self-adapting ability, which initially reduced and then sustained the solution pH in the range of 3.5-5.2. The abundant intrinsic surface Fe(II) of OA-ZVI bm (45.54% vs. 27.52% in ZVI bm , according to Fe 2p XPS profiles) was oxidized by H 2 O 2 and hydrolyzed to generate protons, and the FeC 2 O 4 ·2H 2 O shell favored the fast transfer of protons to inner Fe 0 , therefore, the consumption-regeneration cycle of protons were accelerated to drove the production of Fe(II) for Fenton reactions, demonstrated by the more prominent H 2 evolution and nearly 100% H 2 O 2 decomposition by OA-ZVI bm . Furthermore, the FeC 2 O 4 ·2H 2 O shell was stable and slightly decreased from 1.9% to 1.7% after the Fenton reaction. This study clarified the significance of proton transfer on the reactivity of ZVI, and provided an efficient strategy to achieve the highly efficient and robust heterogeneous Fenton reaction of ZVI for pollution control., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background and Aims: Hepatic iron overload always leads to oxidative stress, which has been found to be involved in the progression of liver disease. However, whether iron disorder is involved in acute liver disease and the further molecular mechanisms remain unclear. Methods: A mice model of acute liver injury (ALI) was established via intraperitoneal injection of thioacetamide (TAA) (250 mg/kg/day) for 3 consecutive days. Ferrostatin-1 (Fer-1) was administered intraperitoneally (2.5 μM/kg/day) starting 3 days before TAA treatment. Deferoxamine (DFO) was intraperitoneally injected (200 mg/kg/day) with TAA treatment for 3 days. We further observed the effect of Fer-1 on TAA model with high-iron diet feeding. ALI was confirmed using histological examination and liver function activity. Moreover, expressions of iron metabolism and ferroptosis proteins were measured by Western blot analysis. Results: The study revealed that the iron accumulation and ferroptosis contributed to TAA-induced ALI pathogenesis. TAA induced prominent inflammation and vacuolar degeneration in the liver as well as liver dysfunction. In addition, protein expression of the cystine/glutamate antiporter SLC7A11 (xCT) and glutathione peroxidase 4 (GPX4) was significantly decreased in the liver, while transferrin receptor 1 (TfR1), ferroportin (Fpn) and light chain of ferritin (Ft-L) expression levels were increased after TAA exposure. As the same efficiency as DFO, pre-administration of Fer-1 significantly decreased TAA-induced alterations in the plasma ALT, AST and LDH levels compared with the TAA group. Moreover, both Fer-1 and DFO suppressed TfR1, Fpn and Ft-L protein expression and decreased iron accumulation, but did not affect xCT or GPX4 expression in the liver. Both Fer-1and DFO prevented hepatic ferroptosis by reducing the iron content in the liver. Furthermore, Fer-1 also reduced iron and reversed liver dysfunction under iron overload conditions. Conclusion: These findings indicate a role of TAA-induced iron accumulation and ferroptosis in the pathogenesis of ALI model. The effect of Fer-1 was consistent with that of DFO, which prevented hepatic ferroptosis by reducing the iron content in the liver. Thus, Fer-1 might be a useful reagent to reverse liver dysfunction and decreasing the iron content of the liver may be a potential therapeutic strategy for ALI. [ABSTRACT FROM AUTHOR]

Heterogeneous peroxydisulfate (PDS) activation driven by conventional electron transfer (ET) is often frustrated by low thermodynamic driving force and sluggish kinetics. Herein, we propose a proton-coupled electron transfer (PCET) strategy of PDS activation, by utilizing ball-milled phosphorylated zero-valent iron (P-ZVIbm) as a PCET platform. P-ZVIbm efficiently activated PDS to produce SO 4 •− and •OH for rapid degradation of 4-chlorophenol in a wide pH range of 3.5–10.5, with rate constants 3–62 times those of the ZVIbm/PDS counterpart. PCET mechanism was evidenced by the pH dependent kinetics, kinetic isotope effect, and proton inventory study. The surface-bound phosphates offer flexible pendant protons (P-O-H) through hydrogen bonds, delocalizing electrons of peroxide O to polarize the O-O bond, thereby facilitating the ET from ZVI for O-O bond cleavage. The work demonstrates the superiority of PCET strategy for heterogeneous PDS activation, and shall guide the design of high-performance Fenton-like catalysts. [Display omitted] • PCET significantly promotes the thermodynamics and kinetics of PDS activation. • P-ZVIbm serves as a proof-of-concept PCET platform of PDS activation. • ZVI, water and phosphate are electron/proton donors and proton relay, respectively. • Phosphate offers flexible pendant protons to the O-O of PDS through hydrogen bond. • P-ZVIbm/PDS rapidly removes 4-CP from water over a wide pH range. [ABSTRACT FROM AUTHOR]

• ZVI/H2O2 delivers a controllable reduction-oxidation coupling process for CNBs remediation. • ZVI pre-reduction significantly accelerates CNBs mineralization rate by ·OH. • The performance of ZVI/H2O2 based reduction-oxidation process is controlled by the addition time of H2O2. • The efficiency of this controllable reduction-oxidation process has been validated in remediating real site contaminated by CNBs. Chloronitrobenzenes (CNBs) are typical refractory aromatic pollutants. The reduction products of CNBs often possess higher toxicity, and the electron-withdrawing substituent groups are detrimental to the ring-opening during the oxidation treatment, leading to ineffective removal of CNBs by either reduction or oxidation technology. Herein we demonstrate a controllable reduction-oxidation coupling (ROC) process composed of zero-valent iron (ZVI) and H 2 O 2 for the effective removal of CNBs from both water and soil. In water, ZVI first reduced p-CNB into 4-chloronitrosobenzene and 4-chloroaniline intermediates, which were then suffered from the subsequent oxidative ring-opening by ·OH generated from the reaction between Fe(II) and H 2 O 2. By controlling the addition time of H 2 O 2 , the final mineralization rate of p-CNB reached 6.6 × 10−1 h−1, about 74 times that of oxidation alone (9.0 × 10−3 h−1). More importantly, this controllable ROC process was also applicable for the site remediation of CNBs contaminated soil by either ex-situ treatment or in-situ injection, and, respectively decreased the concentrations of p-CNB, m-CNB, and o-CNB from 1105, 980, and 94 mg/kg to 3, 1, and < 1mg/kg, meeting the remediation goals (p-CNB: < 32.35 mg/kg, o-CNB and m-CNB: < 1.98 mg/kg). These laboratory and field trial results reveal that this controllable ROC strategy is very promising for the treatment of electron-withdrawing groups substituted aromatic contaminates. [Display omitted] [ABSTRACT FROM AUTHOR]