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Updated: Aug 5, 2026

Preparation of Polyoxometalate-based Photo-responsive Membranes for the Photo-activation of Manganese Oxide Catalysts
Published on: August 7, 2018
Fe/Mo bimetallic oxide nanozyme achieves self-sufficient ROS cascade catalysis for cancer catalytic therapy
Zipeng Liu1, Xuan Liu1, Jiaqi Wei1
1College of Basic Medical Science, Key Laboratory of Pathogenesis Mechanism and Control of Inflammatory-autoimmune Diseases of Hebei Province, State Key Laboratory of New Pharmaceutical Preparations and Excipients, Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education, Hebei University, Baoding 071002, PR China.
Abstract:
Reactive oxygen species (ROS)-mediated catalytic therapy represents a promising candidate for tumor treatment, yet most current systems rely on external energy stimulation or exogenous substrates, limiting therapeutic efficiency in the heterogeneous tumor microenvironment (TME). Herein, we report a Fe/Mo bimetallic oxide nanozyme supported by carbon nanospheres (Fe₂(MoO₄)₃/C) that achieves self-sufficient ROS cascade catalysis for efficient cancer catalytic therapy. The nanozyme simultaneously exhibits superoxide dismutase (SOD)-like and peroxidase (POD)-like activities, enabling autonomous ROS amplification entirely driven by endogenous tumor microenvironment components. Specifically, endogenous superoxide anion (•O₂-) is catalytically converted into H₂O₂ via SOD-like activity, followed by POD-like conversion of H₂O₂ into highly cytotoxic hydroxyl radicals (•OH) under acidic TME conditions, thereby establishing a substrate self-sufficient ROS cascade without exogenous H₂O₂ supplementation or external stimulation. Fe₂(MoO₄)₃/C demonstrated markedly enhanced catalytic kinetics and ROS amplification compared with monometallic counterparts, resulting in pronounced oxidative stress, tumor cell apoptosis, and proliferation inhibition. In a 4T1 breast tumor model, the nanozyme achieved significant tumor growth suppression while exhibiting a favorable safety under the present experimental conditions. This work establishes a self-sufficient catalytic mechanism for continuous ROS amplification and provides a promising strategy for precise and efficient tumor catalytic therapy.
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