Jinsheng Shi

Ferric phosphate (FePOs) nanoenzymes can express peroxidase (POD) activity under the dual stimulation of an acidic environment and high H₂O₂ concentrations. In living organisms, this generates reactive oxygen species (ROS) in sites of lesion infection, and thus FePOs nanoenzymes can act as antimicrobial agents. Here, CeO₂ and ZnO₂ were immobilized in a scallop-type FePOs nanoenzyme material loaded with a photosensitizer, indocyanine green, to synthesize a multifunctional cascade nanoparticle system (FePOs-CeO₂-ZnO₂-ICG, FCZI NPs). H₂O₂ concentrations could be adjusted through the ZnO₂ self-activation response to the slightly acidic environment in biofilms, further promoting the release of ROS from the POD-like reaction of FePOs, achieving amplification of oxidative stress, DNA and cell membrane damage, and exploiting the photodynamic/photothermal effects of indocyanine green to enhance the antibiofilm effects. CeO₂ can remove redundant ROS by switching from Ce⁴⁺ to Ce³⁺ valence, enhancing its ability to fight chronic inflammation and oxidative stress and thus promoting the regeneration of tissues around infection. By maintaining the redox balance of normal cells, increasing ROS at the infection site, eliminating redundant ROS, and protecting normal tissues from damage, the synthesized system maximizes the elimination of biofilms and treatment at the infection site. Therefore, this work may pave the way for the application of biocompatible nanoenzymes.

Intracellular zinc ion (Zn²⁺) accumulation disrupts the Zn²⁺ homeostasis, providing an ion‐overloading anticancer strategy with great potential. The self‐adaptation of tumor cells to ion concentration, however, puts forward higher requirements for the design of ion‐overloading strategy. Herein, “block and attack” antitumor strategy was applied through a composite nanomaterials (UHSsPZH NPs). The strategy demonstrated powerful ion interference ability through both “blocking” the efflux of excess Zn²⁺ via gene silencing and “attacking” tumor cells via target delivery of ZnO₂. After cellular internalization, ZnO₂ was degraded to Zn²⁺ and hydrogen peroxide (H₂O₂), and the gene expression of zinc transporter 1 (ZnT1) was silenced by targeting of released siRNA, which together caused intracellular Zn²⁺‐overload. Disorder of Zn²⁺ further interfered with intracellular Ca²⁺ homeostasis, inhibited the electron transport chain and promoted the production of endogenous reactive oxygen species (ROS), which assisted the “attack” to tumor cells together with the exogenous ROS generated by UHSsPZH NPs under 980 nm laser irradiation. In summary, this work supplies a “block and attack” strategy for the application of ion homeostasis interference in tumor therapy.

Three-dimensional (3D) photocatalysts can overcome the serious aggregation exhibited by two-dimensional (2D) nanosheets caused by unavoidable van der Waals forces. However, the water splitting efficiency needs further improvement, which can be achieved by boosting the exciton dissociation and charge transfer. Herein, a gelatin-confined strategy is developed to construct 3D tube-assembled g-C₃N₄ open frameworks. The gelatin plays multiple roles in the thermal polymerization. It not only engineers the grain growth of g-C₃N₄, but also supplies in situ external C and O sources. Experimental and density functional theory (DFT) calculation results indicate that the self-integration effects of the unique 3D architecture and bridging electron delocalization channels lead to prompt exciton production and dissociation, and subsequent carrier transfer. Consequently, the g-C₃N₄ open framework achieves a hydrogen evolution rate of 99.4 μmol h⁻¹ and an apparent quantum efficiency of 7.43% at 450 nm, significantly superior to previously reported C and (or) O-doped 2D g-C₃N₄ and other 3D g-C₃N₄ materials. These findings provide promising guidance for designing efficient 3D architectures to drive photocatalysis and support the broader application of cost-effective biopolymers.

Enhanced photocatalytic H ₂ evolution by bimetal cocatalyst of NiCoP@C.

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, ClO₂-loaded nanoparticles (fluvastatin sodium&metformin&bupivacaine&ClO₂@CaSiO₃@MnO₂-arginine-glycine-aspatic acid (RGD) ([email protected]) NPs) were prepared for synergistic chlorine treatment and methionine-depletion starvation therapy. After outer layer MnO₂ was degraded in the high glutathione (GSH) tumor microenvironment (TME), [email protected] 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 (ClO₂), 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 ClO₂-loaded [email protected] 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.