Huang Peng Adv. Mater, Shenzhen University: Nanocatalysis platform that consumes glutathione and enhances the production of reactive oxygen species for tumor treatment

Chemokinetic Therapy (CDT) is an emerging treatment method that kills cancer cells by converting intracellular hydrogen peroxide (H2O2) into highly toxic hydroxyl radicals (•OH). In order to overcome the current shortage of endogenous H2O2 in tumor cells and the limitation that high concentrations of glutathione (GSH) will consume OH, Professor Huang Peng of Shenzhen University has developed a smart nanocatalytic therapy drug PGC-DOX), which has its own The characteristics of supplying H2O2 and consuming GSH can be used for effective treatment of cancer.

Key points of this article:

(1) The experiment uses a simple one-step biomineralization method, using polyethylene glycol modified glucose oxidase (GOx) as a template to form degradable copper-doped calcium phosphate nanoparticles, and then use them to load doxorubicin (DOX) And built the nano platform. Among them, as an enzyme catalyst, GOx can effectively catalyze the production of H2O2 from glucose in cells, which not only makes tumor cells starved , but also provides H2O2 for subsequent Fenton-like reactions.

(2) At the same time, the released Cu2+ ions will undergo redox reactions with intracellular GSH, induce GSH depletion and reduce Cu2+ to the Fenton reaction reagent Cu+ ions, and then convert H2O2 to OH through the Cu+-mediated Fenton-like reaction. So as to achieve CDT. Because the platform integrates GOx-mediated starvation treatment, self-supply of H2O2 and GSH-enhanced CDT, and DOX-induced chemotherapy and other therapeutic strategies, PGC-DOX can effectively inhibit tumor growth in vivo, and will not produce obvious side effect.

references:

Lian-Hua Fu. et al. Nanocatalytic Theranostics with Glutathione Depletion and Enhanced Reactive Oxygen Species Generation for Efficient Cancer Therapy. Advanced Materials 2021.

DOI: 10.1002/adma.202006892

https://onlinelibrary.wiley.com/doi/full/10.1002/adma.202006892