Conventional heteroatom-doped graphene oxide (GO) nanozymes usually suffer from complicated manufacturing processes and difficult recovery of nanozymes. Herein, a facile and ecofriendly approach is developed to write nitrogen- and boron-codoped GO nanozyme patterns on a flexible plastic film by CO2 laser scanning in ambient air without any catalyst, mask, or template. The resulting N-doped laser-induced graphene (LIG) with a hierarchical porous and hydrophilic interface possesses intrinsic peroxidase-like activities in catalyzing the typical chromogenic reaction of 3,3′,5,5′-tetramethylbenzidine, denoted as N-doped LIG nanozyme (N-LIGzyme). Further compositional modification with boron atoms doped into N-LIGzyme (N,B-LIGzyme) produces a significant and specific enhancement for the peroxidase-mimetic activity with good reproducibility, high stability, and acceptable recyclability. Owing to the high peroxidase-like activity of N,B-LIGzyme that could convert H2O2 into a hydroxyl radical (•OH), N,B-LIGzyme shows enhanced bactericidal ability against both Gram-negative (Escherichia coli) and Gram-positive (Staphylococcus aureus) bacteria. It is expected that the proposed facile and green synthesis of N,B-LIGzyme atop flexible plastic films will not only open up an exciting vista in the novel applications of classical LIG but also provide a new avenue to design flexible nanozymes with excellent catalytic activity, good operational stability, and easy separation.

During rapid proliferation and metabolism, tumor cells show a high dependence on methionine. The deficiency of methionine exhibits significant inhibition on tumor growth, which provides a potential therapeutic target in tumor therapy. Herein, ClO 2 -loaded nanoparticles (fluvastatin sodium&metformin&bupivacaine&ClO 2 @CaSiO 3 @MnO 2 -arginine-glycine-aspatic acid (RGD) (MFBC@CMR) NPs) were prepared for synergistic chlorine treatment and methionine-depletion starvation therapy. After outer layer MnO 2 was degraded in the high glutathione (GSH) tumor microenvironment (TME), MFBC@CMR NPs released metformin (Me) to target the mitochondria, thus interfering with the tricarboxylic acid (TCA) cycle and promoting the production of lactate. In addition, released fluvastatin sodium (Flu) by the NPs acted on monocarboxylic acid transporter 4 (MCT4) in the cell membrane to inhibit lactate leakage and induce a decrease of intracellular pH, further prompting the NPs to release chlorine dioxide (ClO 2 ), which then oxidized methionine, inhibited tumor growth, and produced large numbers of Cl − in the cytoplasm. Cl − could enter mitochondria through the voltage-dependent anion channel (VDAC) channel, which was opened by bupivacaine (Bup). The disruption of Cl − homeostasis promotes mitochondrial damage and membrane potential decline, leading to the release of cytochrome C (Cyt-C) and apoptosis inducing factor (AIF) and further inducing cell apoptosis. To sum up, the pH-regulating and ClO 2 -loaded MFBC@CMR nanoplatform can achieve cascade chlorine treatment and methionine-depletion starvation therapy toward tumor cells, which is of great significance for improving the clinical tumor treatment effect.