Excess Peroxide Research Articles

Mechanisms for the Production and Suppression of Hydrogen Peroxide at the Hydrogen Electrode in Proton Exchange Membrane Fuel Cells and Water Electrolyzers: Theoretical Considerations

Hydrogen peroxide is inevitably produced at the hydrogen electrode in both the proton exchange membrane fuel cell (PEMFC) and the proton exchange membrane water electrolyzer (PEMWE) when platinum-based catalysts are used. This peroxide attacks and degrades the membrane, seriously limiting its lifetime. Here we review some of our previous efforts to suppress peroxide production using PtFe as a hydrogen evolution reaction (HER) catalyst and PtCo as a hydrogen oxidation reaction (HOR) catalyst. The mechanisms, which involve the chemical reaction of adsorbed hydrogen with oxygen, are examined using density functional theory. The onset of excess peroxide production at 0.1 V above the reversible potential has not been adequately explained thus far, and therefore a new mechanism is proposed here. This involves a unique reaction site including hydrogen adsorbed at (110) step edges adjacent to (111) terraces on the Pt surface, as well as on Pt alloys and other metals such as Rh and Ir. This mechanism helps explain the recent finding of the Wadayama group that Ir single crystal surfaces such as Ir(111) and Ir(110) produce little peroxide during the HOR. It also points the way toward the design of new catalysts for the hydrogen electrode that suppress peroxide production while retaining high HOR and HER activity.

Oxygen/Nitric Oxide Dual-Releasing Nanozyme for Augmenting TMZ-Mediated Apoptosis and Necrosis.

Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor, with a poor prognosis. Temozolomide (TMZ) represents the standard chemotherapy for GBM but has limited efficacy due to poor targeting and a hypoxic tumor microenvironment (TME). To address these challenges, we developed a dual-gas-releasing, cancer-cell-membrane-camouflaged nanoparticle to deliver TMZ. This nanoceria, camouflaged with a cancer cell membrane (CCM-CeO2), targets explicitly GBM cells and accumulates in lysosomes, triggering the rapid release of TMZ. Additionally, CCM-CeO2 could release oxygen (O2) and nitric oxide (NO) in response to the TME. Synthesized using d-arginine, catalytic nanoceria could decompose excessive hydrogen peroxide (H2O2) in the TME to produce O2, while d-arginine could nonenzymatically react with H2O2 to generate NO. CCM-CeO2 could penetrate GBM spheroids to a depth of 148.3 ± 31 μm, with the O2 and NO produced, reducing HIF-1α protein expression. When loaded with TMZ, CCM-CeO2 could increase the intracellular ROS produced by TMZ, leading to lysosome membrane permeabilization and notably augmented apoptosis and necrosis in GBM cells. An in vitro antitumor assay using spheroids showed that CCM-CeO2 reduced the IC50 value of TMZ from 174.5 to 42.6 μg/mL, likely due to the catalase-like activity of nanoceria. These results suggest that alleviating hypoxia and increasing ROS produced by chemotherapeutics could be an effective therapeutic strategy for treating GBM.

Fe/Cu Bimetallic Nanozyme Co-Assembled with 177Lu and Tanshinone for Quadruple-Synergistic Tumor-Specific Therapy.

The co-loading of radionuclides and small-molecule chemotherapeutic drugs as nanotheranostic platforms using nanozymes holds tremendous potential for imaging-guided synergistic therapy. This study presents such nanotheranostic platform (177Lu-MFeCu@Tan) via co-assembling 177Lu radionuclide and tanshinone (Tan) into Fe/Cu dual-metal nanozyme (MFeCu). This platform simultaneously enables single-photon emission computed tomography (SPECT) imaging and a quadruple-synergistic tumor therapy approach, including internal radioisotope therapy (RIT), catalysis therapy, chemotherapy, and MFeCu-mediated ferroptosis and cuproptosis therapy. In this platform, the MFeCu can catalyze excessive intracellular hydrogen peroxide (H2O2) to generate radical oxygen species (ROS) and deplete glutathione (GSH). The excess of H2O2 and GSH are main factors for radioresistance and chemoresistance, reducing them can enhance chemotherapy and RIT. The generated ROS and depleted GSH further induce mitochondrial dysfunction and promote the aggregation of lipoylated dihydrolipoamide S-acetyltransferase and lipid peroxidation, causing the enhance of ferroptosis and cuproptosis. The in vitro and in vivo results demonstrate that this quadruple-synergistic approach shows significant therapeutic efficacy to complete tumor eradication and reduced recurrence in vivo. In conclusion, this work presents a promising strategy for designing SPECT imaging-guided quadruple-synergistic therapy and highlights the feasibility of developing a self-assembled radionuclide and small molecule chemotherapy drugs nanotherapeutic platform for combined treatment of cancer.

SOD1 Is an Integral Yet Insufficient Oxidizer of Hydrogen Sulfide in Trisomy 21 B Lymphocytes and Can Be Augmented by a Pleiotropic Carbon Nanozyme.

Down syndrome (DS) is a multisystemic disorder that includes accelerated aging caused by trisomy 21. In particular, overexpression of cystathionine-β-synthase (CBS) is linked to excess intracellular hydrogen sulfide (H2S), a mitochondrial toxin at higher concentrations, which impairs cellular viability. Concurrent overexpression of superoxide dismutase 1 (SOD1) may increase oxidative stress by generating excess hydrogen peroxide (H2O2) while also mitigating the toxic H2S burden via a non-canonical sulfide-oxidizing mechanism. We investigated the phenotypic variability in basal H2S levels in relation to DS B lymphocyte cell health and SOD1 in H2S detoxification. The H2S levels were negatively correlated with the DS B lymphocyte growth rates but not with CBS protein. Pharmacological inhibition of SOD1 using LCS-1 significantly increased the H2S levels to a greater extent in DS cells while also decreasing the polysulfide products of H2S oxidation. However, DS cells exhibited elevated H2O2 and lipid peroxidation, representing potential toxic consequences of SOD1 overexpression. Treatment of DS cells with a pleiotropic carbon nanozyme (pleozymes) decreased the total oxidative stress and reduced the levels of the H2S-generating enzymes CBS and 3-mercaptopyruvate sulfurtransferase (MPST). Our results indicate that pleozymes may bridge the protective and deleterious effects of DS SOD1 overexpression on H2S metabolism and oxidative stress, respectively, with cytoprotective benefits.

A Multi-Enzyme Nanocascade to Target Disease-Relevant Metabolites.

Metabolic processes in living organisms depend on the synergistic actions of enzymes working in proximity and in concert, catalyzing reactions effectively while regulating the formation of metabolites. This enzyme synergy offers promising therapeutic application for diseases such as alcohol intoxication, cancer, and hyperinflammation. Despite their potential, the clinical translation of enzyme cascades is restricted by challenges including poor enzyme stability, short half-life, and a lack of delivery strategies that maintain enzyme proximity. In this study, multi-enzyme nanocascades synthesized are developed through in situ atom transfer radical polymerization using a zwitterionic monomer. This method markedly enhances enzyme stability and proximity, thereby prolonging their circulation half-life after systemic administration. It is demonstrated that the nanocascades of uricase and catalase effectively reduce uric acid levels without excessive hydrogen peroxide production, providing a potential antidote for hyperuricemia. Moreover, in a murine breast cancer model, the nanocascades of glucose oxidase and catalase inhibited tumor progression and enhanced the therapeutic efficacy of doxorubicin. The prolonged circulation and promoted reaction efficacy of these nanocascades underscore their substantial potential in enzyme replacement therapy and the treatment of various diseases.

Separation of cerium from solution by oxidative precipitation with hydrogen peroxide: The reaction mechanism

Cerium removal from solution via oxidative precipitation with hydrogen peroxide was investigated in a batch reactor to identify optimum conditions for maximum Ce removal. Tests were performed under ambient temperature at pH 2, 3, 4 and 5, using the exact stoichiometric requirement and 30 % and 50 % excess, respectively. It was found that, unlike the usual direct Ce(OH)4 formation presented in the literature for most oxidants, the reaction with hydrogen peroxide proceeded via a metastable ceric hydroxide, with conversion rates increased by increasing temperature. Standard free energies of reaction were calculated for both routes. To better understand the process, the oxidation of Ce(III) to Ce(IV) and the precipitation of Ce(OH)4 were studied separately via a decoupled approach at low pH and reaction mechanisms for each process were proposed. The Ce(III) oxidation reaction was identified as the rate-limiting step, whereas Ce(IV) precipitation was fast and quantitative. In the pH range of 3–5, Ce removal extents varied between 80 and 95 %, depending on the hydrogen peroxide excess. Following the Ce removal step via oxidative precipitation, it was found that a 2 h ageing stage at 80 °C and pH 2.5 was required to complete the transition of cerium hydroxy-peroxide to the more stable ceric hydroxide and decompose any residual H2O2.

Demyelination in cuprizone mice is ameliorated by calycosin mediated through astrocyte Nrf2 signaling pathway

Oxidative stress plays a pivotal role in multiple sclerosis (MS), triggering demyelination predominantly through excessive peroxide production and the depletion of antioxidants. The accumulation of oxidative damage can be caused by dysregulation of astrocytes, which are the brain's main regulators of oxidative homeostasis. Calycosin, an essential bioactive component extracted from Astragalus, is recognized for its neuroprotective properties. Although recent research has highlighted calycosin's neuroprotective capabilities, its role in demyelinating conditions like MS remains unclear. In this work, we examined the possible molecular mechanism of calycosin's neuroprotective effect on cuprizone (CPZ)-induced demylination in mice. According to our research, calycosin successfully reduced demyelination and behavioral dysfuction in CPZ mice. Calycosin also decreased the production of oxidative stress and enhanced the expression of antioxidants in CPZ mice and in astrocytes induced by hydrogen peroxide (H2O2). Furthermore, both in vivo and in vitro experiments demonstrated that calycosin promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) along with the upregulation of heme oxygenase 1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), and superoxide dismutase (SOD). Importantly, the application of all-trans retinoic acid (ATRA), a specific inhibitor of Nrf2, effectively reversed the myelin-protective and antioxidant effects conferred by calycosin. This study suggested that calycosin might exert neuroprotection by inhibiting oxidative stress and reducing demyelination via the activation of astrocyte Nrf2 signaling. These findings indicated that calycosin might be a potential candidate for treating MS.

Self-cleaning electrode for stable synthesis of alkaline-earth metal peroxides.

Alkaline-earth metal peroxides (MO2, M = Ca, Sr, Ba) represent a category of versatile and clean solid oxidizers, while the synthesis process usually consumes excessive hydrogen peroxide (H2O2). Here we discover that H2O2 synthesized via two-electron electrochemical oxygen reduction (2e- ORR) on the electrode surface can be efficiently and durably consumed to produce high-purity MO2 in an alkaline environment. The crucial factor lies in the in-time detachment of in situ-generated MO2 from the self-cleaning electrode, where the solid products spontaneously detach from the electrode to solve the block issue. The self-cleaning electrode is achieved by constructing micro-/nanostructure of a highly active catalyst with appropriate surface modification. In experiments, an unprecedented accumulated selectivity (~99%) and durability (>1,000 h, 50 mA cm-2) are achieved for electrochemical synthesis of MO2. Moreover, the comparability of CaO2 and H2O2 for tetracycline degradation with hydrodynamic cavitation is validated in terms of their close efficacies (degradation efficiency of 87.9% and 93.6% for H2O2 and CaO2, respectively).

Redox homeostasis disruptors enhanced cuproptosis effect for synergistic photothermal/chemodynamic therapy

The combination of chemodynamic therapy (CDT) with photothermal therapy (PTT) is a promising approach to enhance antitumor efficacy of chemotherapeutics. In this paper, we developed novel copper-chelated polydopamine (PDA) nanoparticles (NPs) functionalized with hyaluronic acid (HA) (Cu-PDA-HA NPs) to induce apoptosis and cuproptosis-induced cell death, synergistically combining PTT and CDT. Experimental results revealed that Cu-PDA-HA NPs can respond to excessive glutathione (GSH) and hydrogen peroxide (H2O2) in the tumor microenvironment (TME), which will enable their specific degradation, thereby leading to efficient accumulation of Cu2+ within tumor cells. The released Cu2+ ions were reduced by GSH to generate Cu+, which catalyzed in situ Fenton-like reactions to produce cytotoxic hydroxyl radicals (·OH), disrupting cellular redox homeostasis and promoting apoptosis-related CDT. Meanwhile, the photothermal effect of the Cu-PDA-HA NPs could enhance oxidative stress within the tumor by elevating the temperature and subsequent ·OH production. The enhanced oxidative stress made tumor cells more vulnerable to cuproptosis-induced toxicity. Furthermore, in vivo experiments demonstrated that Cu-PDA-HA NPs can still undergo a temperature increase of 18.9°C following 808 nm near-infrared irradiation (1.0 W/cm2, 5 min). Meanwhile, Cu-PDA-HA NPs were able to induce oligomerization of dihydrolipoamide S-acetyltransferase (DLAT) and down-regulate Fe-S cluster proteins such as ferredoxin (FDX1), thereby activating cuproptosis. Therefore, this study provides a novel approach for designing multifunctional nanoparticles with on-demand Cu2+ release and offers a fresh perspective for exploring synergistic therapeutic strategies involving CDT/PTT/apoptosis/cuproptosis.

Valence-Change MnO2-Coated Arsenene Nanosheets as a Pin1 Inhibitor for Hepatocellular Carcinoma Treatment.

The heterogeneity of hepatocellular carcinoma (HCC) can prevent effective treatment, emphasizing the need for more effective therapies. Herein, we employed arsenene nanosheets coated with manganese dioxide and polyethylene glycol (AMPNs) for the degradation of Pin1, which is universally overexpressed in HCC. By employing an "AND gate", AMPNs exhibited responsiveness toward excessive glutathione and hydrogen peroxide within the tumor microenvironment, thereby selectively releasing AsxOy to mitigate potential side effects of As2O3. Notably, AMPNs induced the suppressing Pin1 expression while simultaneously upregulation PD-L1, thereby eliciting a robust antitumor immune response and enhancing the efficacy of anti-PD-1/anti-PD-L1 therapy. The combination of AMPNs and anti-PD-1 synergistically enhanced tumor suppression and effectively induced long-lasting immune memory. This approach did not reveal As2O3-associated toxicity, indicating that arsenene-based nanotherapeutic could be employed to amplify the response rate of anti-PD-1/anti-PD-L1 therapy to improve the clinical outcomes of HCC patients and potentially other solid tumors (e.g., breast cancer) that are refractory to anti-PD-1/anti-PD-L1 therapy.

Hydroxygenkwanin exerts a neuroprotective effect by activating the Nrf2/ARE signaling pathway

High levels of reactive oxygen species (ROS) have been associated with the progression of neurodegenerative diseases such as Alzheimer's disease. The activation of the NFE2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway may restore the neuron's redox balance and provide a therapeutic impact. Hydroxygenkwanin (HGK), a dominant flavone from Genkwa Flos, has received expanding attention due to its medicinal activities. Our investigation results demonstrated the ability of HGK to protect the PC12 cells from oxidative damage caused by an excessive hydrogen peroxide load. HGK also showed the ability to upregulate a panel of endogenous antioxidant proteins. Further investigations have demonstrated that the neuroprotection mechanism of HGK is dependent on the activation of the Nrf2/ARE signaling pathway. Activating the Nrf2/ARE pathway by HGK reveals a novel mechanism for understanding the pharmacological functions of HGK. These findings suggest that HGK could be considered for further development as an oxidative stress-related neurological pathologies potential therapeutic drug.

Lutein Modulates Cellular Functionalities and Regulates NLRP3 Inflammasome in a H2O2-Challenged Three-Dimensional Retinal Pigment Epithelium Model.

Excessive hydrogen peroxide (H2O2) generated during retinal cell metabolic activity could lead to oxidative degeneration of retinal pigment epithelium (RPE) tissue, a specific pathological process implicated in various retinal diseases resulting in blindness, which can be mitigated by taking dietary antioxidants to prevent inflammation and impaired cellular dysfunction. This study tested the hypothesis that damages induced by oxidative stresses can be mitigated by lutein in a H2O2-challenged model, which was based on an ARPE-19 cell monolayer cultured on three-dimensional (3D)-printed fibrous scaffolds. Pretreating these models with lutein (0.5 μM) for 24 h can significantly lower the oxidative stress and maintain phagocytosis and barrier function. Moreover, lutein can modulate the NLRP3 inflammasome, leading to a ∼40% decrease in the pro-inflammatory cytokine (IL-1β and IL-18) levels. Collectively, this study suggests that the 3D RPE model is an effective tool to examine the capability of lutein to modulate cellular functionalities and regulate NLRP3 inflammation.

Natural product nanozymes of herbal extract galangin in managing hepatocellular carcinoma.

Numerous local herbal extract species have been investigated as potential medicinal ingredients due to their promising anti-cancer properties. However, the primary constraint of the class of plant flavonoids lies in their low solubility and limited membrane permeability, leading to chemical instability and restricted bioavailability that impede biomedical applications. In this study, we have developed an ideal nanozyme-Galazyme, comprising galangin-loaded copper Nanozyme coated by DSPE-PEG, which amplifies oxidative stress to induce apoptosis via the regulation of reactive oxygen species (ROS) generation and mitogen-activated protein kinase (MAPK) activation. Galazyme exhibited significant peroxidase mimetic activity, demonstrating its potential to generate ROS and elevate oxidative stress. Upon uptake by HepG-2 cells, Galazyme efficiently converts excess hydrogen peroxide (H2O2) into highly reactive •OH radicals and upregulates MAPK expression, leading to the activation of Bax and Caspase 3, thereby promoting irreversible tumor cell apoptosis. Both in vitro and in vivo results demonstrate that Galazyme inhibits tumor cell growth and induces apoptosis by generating ample ROS and activating the MAPK pathway. Our study offers novel evidence supporting the enhancement of Galazyme-induced apoptosis through the upregulation of Bax and Caspase 3, along with the elucidation of the interaction between MAPK and apoptosis.

Chitosan-modified manganese oxide-conjugated methotrexate nanoparticles delivering 5-aminolevulinic acid as a dual-modal T1-T2* MRI contrast agent in U87MG cell detection.

Glioblastoma multiforme is a highly aggressive form of brain cancer, and early diagnosis plays a pivotal role in improving patient survival rates. In this regard, molecular magnetic resonance imaging has emerged as a promising imaging modality due to its exceptional sensitivity to minute tissue changes and the ability to penetrate deep into the brain. This study aimed to assess the efficacy of a novel contrast agent in detecting gliomas during MRI scans. The contrast agent utilized modified chitosan coating on manganese oxide nanoparticles. The modification included adding methotrexate and 5-aminolevulinic acid (MnO2/CS@5-ALA-MTX) to target cells with overexpressed folate receptors and breaking down excess hydrogen peroxide in tumor tissue, resulting in enhanced signal intensity in T1-weighted MR images but diminished signal intensity in T2*-weighted MR images. The nanosystem was characterized and evaluated in MR imaging, safety, and ability to target cells both in vivo and in vitro. MTX-free nanoparticles (MnO2/CS@5-ALA NPs) had no obvious cytotoxicity on cell lines U87MG and NIH3T3 after 24/48 h at a concentration of up to 160 µgr/mL (cell viability more than 80%). In this system, methotrexate enables tumor targeting and the MnO2/5-ALA improves T1-T2*-weighted MRI. In addition, MRI scans of mice with M109 carcinoma indicated significant tumor uptake and NP capacity to improve the positive contrast effect. This developed MnO2/CS@5-ALA-MTX nanoparticle system may exhibit great potential in the accurate diagnosis of folate receptor over-expressing cancers such as glioblastoma.

Cascade Nanoreactor Employs Mitochondrial-Directed Chemodynamic and δ-ALA-Mediated Photodynamic Synergy for Deep-Seated Oral Cancer Therapy.

The management of oral squamous cell carcinoma (OSCC) poses significant challenges, leading to organ impairment and ineffective treatment of deep-seated tumors, adversely affecting patient prognosis. A cascade nanoreactor that integrates photodynamic therapy (PDT) and chemodynamic therapy (CDT) for comprehensive multimodal OSCC treatment is introduced. Utilizing iron oxide and mesoporous silica, the FMMSH drug delivery system, encapsulating the photosensitizer prodrug δ-aminolevulinic acid (δ-ALA), is developed. Triphenylphosphine (TPP) modification facilitates mitochondrial targeting, while tumor cell membrane (TCM) coating provides homotypic targeting. The dual-targeting δ-ALA@FMMSH-TPP-TCM demonstrate efficacy in eradicating both superficial and deep tumors through synergistic PDT/CDT. Esterase overexpression in OSCC cells triggers δ-ALA release, and excessive hydrogen peroxide in tumor mitochondria undergoes Fenton chemistry for CDT. The synergistic interaction of PDT and CDT increases cytotoxic ROS levels, intensifying oxidative stress and enhancing apoptotic mechanisms, ultimately leading to tumor cell death. PDT/CDT-induced apoptosis generates δ-ALA-containing apoptotic bodies, enhancing antitumor efficacy in deep tumor cells. The anatomical accessibility of oral cancer emphasizes the potential of intratumoral injection for precise and localized treatment delivery, ensuring focused therapeutic agent delivery to maximize efficacy while minimizing side effects. Thus, δ-ALA@FMMSH-TPP-TCM, tailored for intratumoral injection, emerges as a transformative modality in OSCC treatment.

Smartphone-Integrated Automated Sensor Employing Electrochemically Engineered 3D Bimetallic Nanoflowers for Hydrogen Peroxide Quantification in Milk.

Hydrogen peroxide (H2O2), one of the reactive oxygen species in living beings, serves as a regulator of various cellular processes. However, excessive peroxide concentrations are linked to oxidative stress and promptly disrupt cellular components, leading to several pathological conditions in the body. Moreover, it is extremely reactive and has a limited lifetime; thus, H2O2 sensing remains a prominent focus of research. Enzymatic sensing probes were widely employed to detect H2O2 in the recent past; however, they are susceptible to intrinsic chemical and thermal instabilities, which decrease the reliability and durability of the surface. This research was designed to come up with a feasible solution to this problem. Herein, a novel nonenzymatic peroxidase-mimic three-dimensional (3D) bimetallic nanoflower has been synergistically engineered for quick sensing of H2O2. The sensor platform showed minimal resistance or enhanced charge transfer properties as well as remarkable analytical capability, having a broad linear range between 0.01 and 1 nM and a detection limit of 1.46 ± 0.07 pM. The probe responded to changes in H2O2 concentration in just 2.10 ± 0.02 s, making it a quick sensing platform for H2O2 tracking. This peroxidase-mimic nanozyme probe showed minimal sensitivity to interferants often seen in real-world sample matrices and possessed good recoveries ranging from 92.88 to 99.09% in milk samples. Further, a facile and user-friendly smartphone application (APP) named "HPeroxide-Check" was developed and integrated into the sensor to check the milk adulteration by detecting H2O2. It processes the current output obtained from the sensing interface and provides real-time peroxide concentrations in milk. The entire procedure of fabricating the probe is a single, highly robust step that takes only 10 min and is coupled with a smartphone APP, highlighting the sensor's quick manufacturing and deployment for automated H2O2 monitoring in industrial and point-of-care settings.

A nano-oxygen generator for enhanced light-controlled elimination of anaerobic bacteria in periodontal infections

Using nanomaterials with photodynamic therapy (PDT) to combat bacterial infections including periodontal infections has attracted the attention of researchers because of their high efficiency, simplicity and low susceptibility to drug resistance. However, the therapeutic effectiveness is threatened by the endogenous accumulation of hydrogen peroxide and insufficient amounts of the substrate oxygen. Here, we report a microporous Zr porphyrin carboxylate metal-organic framework (MOF) PCN-222 doped with platinum nanozymes, Pt@PCN-222, to reshape the microenvironment that is not conducive to the recovery of infected tissue and further promote recovery after periodontal tissue infection. This MOFdoped with platinum nanozymes can remove excessive endogenous hydrogen peroxide and produce dissolved oxygen simultaneously. This framework can effectively alleviate anaerobic bacterial infection in periodontal tissue, including efficiently killing the bacteria and reducing the level of inflammation in tissue. This work provides a new strategy to solve the long-term clinical challenge of anaerobic bacterial infections in periodontal tissue and proposes an innovative approach to improve treatment.

Tumor Microenvironment Activatable Nanoprodrug System for In Situ Fluorescence Imaging and Therapy of Liver Cancer.

The development of new imaging and treatment nanoprodrug systems is highly demanded for diagnosis and therapy of liver cancer, a severe disease characterized by a high recurrence rate. Currently, available small molecule drugs are not possible for cancer diagnosis because of the fast diffusion of imaging agents and low efficacy in treatment due to poor water solubility and significant toxic side effects. In this study, we report the development of a tumor microenvironment activatable nanoprodrug system for the diagnosis and treatment of liver cancer. This nanoprodrug system can accumulate in the tumor site and be selectively activated by an excess of hydrogen peroxide (H2O2) in the tumor microenvironment, releasing near-infrared solid-state organic fluorescent probe (HPQCY-1) and phenylboronic acid-modified camptothecin (CPT) prodrug. Both HPQCY-1 and CPT prodrugs can be further activated in tumor sites for achieving more precise in situ near-infrared (NIR) fluorescence imaging and treatment while reducing the toxic effects of drugs on normal tissues. Additionally, the incorporation of hydrophilic multivalent chitosan as a carrier effectively improved the water solubility of the system. This research thus provides a practical new approach for the diagnosis and treatment of liver cancer.

Comparison of antimicrobial properties of inorganic peroxide polymer composites

AbstractWound healing and prevention of bacterial infections are critical aspects of modern medical care. In this work, antibacterial films were produced by creating composites of polycaprolactone with inorganic peroxides. Calcium, magnesium, and zinc peroxide were incorporated in a biocompatible polymeric film. Iron oxide, sodium bicarbonate, and calcium phosphate were added to reduce hydrogen peroxide and to maintain pH in a less alkaline range, allowing for optimization of the material's antibacterial efficacy while minimizing cytotoxicity toward human fibroblasts. Experiments with common wound pathogens, Staphylococcus aureus and Pseudomonas aerugonisa, confirmed significant and prolonged antibacterial effects of peroxide‐doped films. Findings showed that the addition of CaO2 and MgO2 within the film increased cytotoxicity toward human fibroblasts after 48 h (30%–40% decrease compared to control), whereas ZnO2‐based films exhibited a minimal cytotoxicity consistently maintaining over 70% cell viability throughout the course of the experiment. We examined the materials’ sustained release of reactive oxygen species and oxygen, and pH variation correlated with antibacterial activity. Given the unique combination of antibacterial efficacy and mammalian biocompatibility, these peroxides have value as components to sustain hydrogen peroxide release when appropriately compounded to reduce pH variation and avoid excessive hydrogen peroxide levels.

Alleviating sweetpotato salt tolerance through exogenous glutathione and melatonin: A profound mechanism for active oxygen detoxification and preservation of photosynthetic organs

Salt stress profoundly impacts sweetpotato production. Exogenous glutathione (GSH) and melatonin (MT) promoted plant growth under stress, but their specific roles and mechanisms in sweetpotato salt tolerance need exploration. This study investigated GSH and MT’s regulatory mechanisms in sweetpotato under salt stress. Salt stress significantly reduces both growth and biomass by hindering photosynthesis, root traits, K+ content, and K+/Na+ balance, leading to oxidative stress and excessive hydrogen peroxide (H2O2), superoxide ion (O2•−), and malondialdehyde (MDA) production and Na+ accumulation. Nevertheless, GSH (2 mM) and MT (25 μM) pre-treatments effectively mitigated salt-induced oxidative damage and protected the plasma membrane. They reduced osmotic pressure by enhancing K+ uptake, K+/Na+ regulation, osmolyte accumulation, and reducing Na+ accumulation. Improved stomatal traits, chloroplast and grana lamella preservation, and maintenance of mesophyll cells, cell wall, and mitochondrial structure were observed with GSH and MT pre-treatments under salt stress, therefore boosting the photosynthetic system and enhancing plant growth and biomass. Moreover, the findings also indicate that the positive outcomes of GSH and MT pre-treatments result from elevated antioxidant levels, enhanced enzymatic activity, and upregulated expression of sodium hydrogen exchanger 2 (NHX2), K+transporter 1 (AKT1), and cation/H+exchanger (CHX), CBL-interacting protein kinase 1 (CIPK1), and antioxidant enzyme genes. These mechanisms enhance structural stability in photosynthesis and reduce salt stress. Evidently, MT pre-treatment exhibited superior effects compared to GSH. These findings provide a firm theoretical basis for employing GSH and MT to enhance salt tolerance in sweetpotato cultivation.