Yulin Huang,Xike Tian,Yulun Nie,Chao Yang,Yanxin Wang
Cu(II) doped mesoporous MnO 2 (Cu-MnO 2 ) was prepared to establish an intimate functional link between the structure substitution and catalytic peroxymonosulfate (PMS) activation. Based on the characterization of powder X-ray diffraction (XRD), N 2 adsorption-desorption measurement, scanning electron microscope (FE-SEM) and transmission electron microscope (TEM), Cu-MnO 2 had a typical long range ordered mesoporous structure and Cu was successfully introduced in octahedral framework. It exhibited excellent catalytic activity and stability for the phenol degradation by PMS. Phenol was always efficiently degraded over Cu-MnO 2 at a pH range of 3.5–9.0. For example, the reaction rate constant at pH 7.0 was 0.073 min −1 , which was two times higher than that of MnO 2 (0.039 min −1 ). Importantly, 1 O 2 was identified as the primary reactive species in Cu-MnO 2 /PMS system. X-ray photoelectron spectroscopy (XPS) confirmed that more exposed surface oxygen defects due to Cu doping were responsible to the enhancement of PMS activation for phenol degradation. The results of PMS decomposition and oxygen evolution indicated that surface oxygen defects lower the reaction energy barrier of PMS decomposition by generating 1 O 2 via the energy trapping by oxygen. Finally, the heterogeneous PMS activation mechanism over Cu-MnO 2 was proposed.
We have developed an innovative Cu-doped and DTX-loaded Cu-MnO2@DTX@FA (MCDF) nanodrug designed to strategically alter tumor microenvironment (TME) by harnessing the synergistic effects of chemodynamic therapy (CDT), chemotherapeutic agents, and the induction of ferroptosis and cuproptosis. The MCDF nanodrug efficiently degrades, releasing abundant Mn4+, Cu2+, and DTX. The conversion of Cu2+ to Cu+ facilitated by FDX1 initiates cuproptosis, while, similar to Mn2+, Cu+ reacts with hydrogen peroxide (H2O2) to generate hydroxyl radicals (·OH). Cu2+ and Mn4+ oxidize glutathione (GSH), significantly depleting GSH levels in tumor cells and inactivating GPX4, which further promotes ferroptosis. The release of Cu2+ and Mn4+ intensifies the cuproptosis. DTX effectively disrupts the cell division cycle, thereby inhibiting the proliferation and spread of tumor cells. The FA-modified MCDF is designed to evade immune detection while selectively targeting tumor tissues, ensuring precision in treatment delivery. This cutting-edge material not only provides a multifunctional therapeutic strategy but also sets the stage for the next generation of tumor-targeting nanomedicines.
Nitrogen-containing polymer-supported Cu-doped MnO 2 (Cu-MnO 2 @PDVTA) nanowires were prepared and their catalytic performances were evaluated via oxidation of biomass-derived 5-hydroxymethylfurfural (HMF) to 2,5-furandicarboxylic acid (FDCA). The Cu-MnO 2 @PDVTA catalysts were characterized by Fourier-transform infrared spectroscopy, X-ray diffraction, N 2 physical adsorption, transmission electron microscopy, and X-ray photoelectron spectroscopy. Both the Cu 2+ and MnO 2 nanoparticles were found to synergistically promote HMF oxidation to FDCA via 2,5-furandicarbaldehyde and 5-formyl-2-furancarboxylic acid intermediates. The Cu-MnO 2 @PDVTA-3 catalyst demonstrated the highest catalytic activity, providing FDCA with an excellent yield of 96.8% after 12 h at 80 °C. The time course of HMF oxidation revealed that oxidation of the hydroxyl group in HMF was easier than that of the aldehyde group. Cu-MnO 2 @PDVTA-3 could act as a reusable heterogeneous catalyst for HMF oxidation.
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