Oxidative Environment Research Articles

A Multifunctional Nanodelivery System Modified by Fusion Peptides Acts as Teriparatide Carrier for Noise-Induced Hearing Loss Therapy.

Noise-induced hearing loss (NIHL) is among the most poorly treated diseases due to irreversible damage to hair cells. Reactive oxygen species contribute to NIHL pathogenesis by injuring the inner ear hair cells. Teriparatide (PTH1-34) exerts antioxidant properties in the context of osteoporosis. Thus, in the current study, a multifunctional thermosensitive nanodelivery system is developed, based on the unique anatomical structure of the inner ear, to load and sustain the release of PTH1-34 to alleviate hair cell damage. LR27-a fusion peptide-is assembled from a targeting peptide (A665) and cell-penetrating peptide (Arg8) to target hair cells and increase the round window membrane permeability. In vitro, the antioxidant and anti-apoptotic properties of the nanodelivery system are assessed after treating HEI-OC1 cells and cochlear explants with hydrogen peroxide to simulate the oxidative environment. In vivo, injection of the nanodelivery system into the auditory bulb protects the hearing and hair cells of an NIHL mouse model. These results demonstrate the synergistic effects of multiple peptides in treating NIHL and their potential clinical applications.

Innovative asymmetric CoSA‐N‐Ti3C2Tx catalysis: unleashing superoxide radicals for rapid self‐coupling removal of phenolic pollutant

The polymerization pathway of contaminants rivals the traditional mineralization pathway in water purification technologies. However, designing suitable oxidative environments to steer contaminants toward polymerization remains challenging. This study introduces a nitrogen‐oxygen double coordination strategy to create an asymmetrical microenvironment for Co atoms on Ti3C2Tx MXenes, resulting in a novel Co‐N2O3 microcellular structure that efficiently activates peroxymonosulfate. This unique activation capability led to the complete removal of various phenolic pollutants within 3 min, outperforming the representative Co single‐atom catalysts reported in the past three years. Identifying and recognizing reactive oxygen species highlight the crucial role of ·O2−. The efficient pollutant removal occurs through a ·O2−‐mediated radical pathway, functioning as a self‐coupling reaction rather than deep oxidation. Theoretical calculations demonstrate that the electron‐rich pollutants transfer more electrons to the catalyst surface, inducing the reduction of dissolved oxygen to ·O2− in the Co‐N2O3 microregion. In a practical continuous flow‐through application, the system achieved 100% acetaminophen removal efficiency in 6.5 h, with a hydraulic retention time of just 0.98 s. This study provides new insights into the previously underappreciated role of ·O2− in pollutant purification, offering a simple strategy for advancing aggregation removal technology in the field of wastewater treatment.

Innovative asymmetric CoSA-N-Ti3C2Tx catalysis: unleashing superoxide radicals for rapid self-coupling removal of phenolic pollutant.

The polymerization pathway of contaminants rivals the traditional mineralization pathway in water purification technologies. However, designing suitable oxidative environments to steer contaminants toward polymerization remains challenging. This study introduces a nitrogen-oxygen double coordination strategy to create an asymmetrical microenvironment for Co atoms on Ti3C2Tx MXenes, resulting in a novel Co-N2O3 microcellular structure that efficiently activates peroxymonosulfate. This unique activation capability led to the complete removal of various phenolic pollutants within 3 min, outperforming the representative Co single-atom catalysts reported in the past three years. Identifying and recognizing reactive oxygen species highlight the crucial role of ·O2-. The efficient pollutant removal occurs through a ·O2--mediated radical pathway, functioning as a self-coupling reaction rather than deep oxidation. Theoretical calculations demonstrate that the electron-rich pollutants transfer more electrons to the catalyst surface, inducing the reduction of dissolved oxygen to ·O2- in the Co-N2O3 microregion. In a practical continuous flow-through application, the system achieved 100% acetaminophen removal efficiency in 6.5 h, with a hydraulic retention time of just 0.98 s. This study provides new insights into the previously underappreciated role of ·O2- in pollutant purification, offering a simple strategy for advancing aggregation removal technology in the field of wastewater treatment.

Design and advances in antioxidant hydrogels for ROS-induced oxidative disease.

Reactive oxygen species (ROS) play a crucial role in human physiological processes, but oxidative stress caused by excessive ROS may lead to a variety of acute and chronic diseases. Despite the development of various strategies and biomaterials, an efficiently and broadly applied method for treatment of ROS-induced oxidative disease remains a bottleneck. Aiming to improve the local oxidative stress environment, numerous bioactive hydrogels with antioxidant properties have emerged and are proven to quickly and continuously eliminate excessive ROS. To deeply understand the design principles and applications of antioxidant hydrogels is highly beneficial for designing antioxidant hydrogels for treatment of oxidative disease. This review provides a detailed summary of recent advances in design and applications of antioxidant hydrogels for various ROS-induced oxidative diseases. In this review, the kinds of antioxidant components in antioxidant hydrogels are outlined in detail. Additionally, the crosslinking methods and the biomedical applications of antioxidant hydrogels are widely summarized and discussed, especially focusing on their usage in different types of diseases and the attention given to the treatment of diseases such as skin wounds, myocardial infarction, and osteoarthritis. Finally, the future development direction of antioxidant hydrogel is further proposed. STATEMENT OF SIGNIFICANCE: Oxidative stress is a pivotal biochemical process that plays a critical role in cellular homeostasis. Excessive cellular oxidative stress triggers an inflammatory response, which is implicated in a spectrum of associated diseases. Given the critical need for managing oxidative stress, antioxidant therapies have become a vital focus in medical research. Hydrogels have garnered substantial interest among biomaterial scientists due to their hydrophilic nature and biocompatibility. The review delves into the realm of antioxidant hydrogels, encompassing the classification of antioxidant components, the synthesis and fabrication of hydrogels, and a comprehensive overview of the biological applications and challenges of these antioxidant hydrogels. Aiming to provide new perspectives for researchers in developing cutting-edge therapeutic approaches that leverage antioxidant hydrogels.

Selective nitric oxide redistribution by phospholipid nanoparticles: A novel strategy to mitigate massive nitric oxide release and prevent reperfusion injury in septic shock.

Nitric oxide plays a critical role in regulating vascular tone, but excessive nitric oxide release during septic shock results in hypotension due to excessive vasodilation and the formation of toxic free radicals. VBI-S is a phospholipid nanoparticle based fluid composed of lipid bilayers formed primarily by phosphatidylcholine and micelles of soybean oil encapsulated by a monolayer of phosphatidylcholine. These nanoparticles offer a novel solution by absorbing and redistributing nitric oxide and nitrite, potentially mitigating the harmful effects of excessive nitric oxide in sepsis. This paper proposes a mechanism in which VBI-S not only redistributes nitric oxide but also reduces ischemia-reperfusion injury by limiting the production and availability of reactive species. VBI-S captures nitric oxide and nitrite in areas of high concentration and redistributes them in low-nitric oxide environments, primarily within oxygen-deprived tissues. Nitrite then contributes to nitric oxide regeneration in hypoxic microvasculature via various reduction pathways, thereby improving tissue perfusion and minimizing oxidative stress. Preliminary studies suggest that nitrite may also decrease reactive species production, primarily superoxide, through the inhibition of mitochondrial complex I. Additionally, the lipid composition of VBI-S is rich in poly and monounsaturated fatty acids which allows VBI-S to act as a substrate for peroxidation via peroxynitrite. Therefore, VBI-S acts as a decoy target thereby protecting cellular membranes from oxidative damage caused by reactive species. These findings position VBI-S as a promising therapeutic agent, offering both nitric oxide regulation and protection against hypotension and toxic free radicals in septic shock patients. Further research is necessary to fully elucidate the molecular pathways and optimize its clinical application.

Subnanometer Tracking of the Oxidation State on Co3O4 Nanoparticles by Identical Location Imaging and Spectroscopy.

Understanding a catalytic reaction requires tools that elucidate the structure of the catalyst surface and subsurface, ideally at atomic resolution and under reaction conditions. Operando electron microscopy meets this requirement in some cases, but fails in others where the required reaction conditions cannot be reached or lead to an unwanted influence of the electron beam on the reactant and catalyst. We introduce ILIAS (identical location imaging and spectroscopy) in combination with a quasi in situ approach to disentangle the effect of heat and gas on the surface of nanoparticles from the effect of the electron beam. With this approach we allow high temperatures and pressures in any gaseous environment on the one hand, and atomic resolution imaging and spectroscopy on the other. As a proof of concept, we resolve the structural evolution of a Co3O4 spinel catalyst using ILIAS and track the oxidation state across the surface before and after heating in a reductive or oxidative environment. We then titrate the surface of the catalyst using CO as a probe molecule to remove highly active oxygen species formed during the thermal treatment, providing unprecedented insight into the interplay between pretreatment and surface reactivity of Co3O4 nanoparticles.

Chromogenic Mechanism and Formation of Zonal Genesis of Raspberry-Red Grossular from the Sierra de Cruces Range, Mexico

The raspberry-red grossular, discovered in the Sierra de Cruces in Coahuila, Mexico, is characterized by its zoned coloration, featuring a pink rim and a black mantle with a sharp color transition at the border. However, there is a notable lack of definitive and systematic identification characteristics pertaining to its special zones. The mineral chemical composition and chromogenic mechanism remain unsupported by empirical validation derived from specific experimental data. In this study, the gemological properties, chemical composition, and spectral characteristics are systematically analyzed to explore the chromogenic mechanism and formation of zonal genesis. The results of the X-ray diffraction pattern, Raman spectrum, and major elements’ composition show that the raspberry-red grossular samples are grossular with high purity. Mn ions are a direct coloring factor of the pink rim of the grossular samples, while Fe ions are chromogenic elements of the black mantle. The MnO content of the pink rim ranges from 0.15 wt% to 1.72 wt%. The FeO content of the black mantle ranges from 3.11 wt% to 5.09 wt%, which is generally higher than that of other parts. The trace element compositions reveal that the rim and core of samples were formed in an oxidative environment (δEu = 0.43–2.41), which could be derived from the hydrothermal metasomatic skarn (δ18O = 11.03–12.14); the mantles of samples were formed in a reducing environment (δEu = 0.42–0.85), which is consistent with the magmatic skarn (δ18O = 11.40–11.66). They also show that the surrounding rocks provide part of the compositional sources for the raspberry-red grossular and interact with the black mantle, which affects the formation of the pink rim. This study offers geological and mineral compositional insights, addressing a significant void in the study of raspberry-red grossular, and lays the foundation for follow-up investigations.

Cycloolefin Copolymers With a Multiply Rigid Structure for Protecting Triplet Exciton From Thermo- and Moisture-Quenching.

Polymeric room temperature phosphorescence (RTP) materials have been well developed and utilized in various fields. However, their fast thermo- and moisture-quenching behavior highly limit their applications in certain harsh environments. Therefore, the preparation of materials with thermo- and moisture-resistant phosphorescence is greatly attractive. Compared with common water-soluble polymers, cycloolefin copolymers (COC) show outstanding hydrophobicity and higher rigidity, even at elevated temperatures, being as a promising candidate to prepare phosphorescence materials with suppressed thermo- and moisture-quenching behavior. Herein, a type of COC bearing hydroxyl, ester, and adamantanyl side groups is synthesized. After dispersing various phosphors into this matrix, the resultant composites exhibit full-color RTP with lifetimes of 249-590 ms. Their luminescence does not show obvious quenching in water, acid, alkalinous, reductive, and oxidative environments. In the presence of both rigid COC matrix and rigid phosphors, the corresponding composite displays high-temperature phosphorescence performance. Even at 378 K, the composite can emit phosphorescence with a lifetime of 40-98 ms. The applications of these COC-based composites for imaging, information encryption, and anti-counterfeiting are thus explored.

P0165 A highly miniaturized ingestible sensor for measuring gut health along the GI tract

Abstract Background The human gastrointestinal (GI) tract is challenging to examine due to its intricate structure and inaccessibility. Current diagnostic methods are either invasive, like endoscopy, or offer a limited view, such as faecal tests. Endoscopy capsules allow for a visual inspection of the whole GI tract but still require uncomfortable bowel preparation, including laxatives and dietary restrictions, and cannot provide biochemical analysis of the gut environment. Methods To enable non-invasive assessment of in vivo gut health, we developed a highly miniaturized, ultra-low-power ingestible sensor (the Gastrointestinal Smart Module, or GISMO) capable of measuring pH, temperature, and redox balance throughout the GI tract. Redox balance is crucial for maintaining intestinal barrier function and regulating interactions among the host, immune system, and gut microbiota. Imbalances in redox levels can lead to oxidative stress, characterized by an imbalance between oxidants and antioxidants, and are associated with adverse gut processes, such as inflammation1. Redox balance plays as such an important role in inflammatory bowel disease (IBD)2. The GISMO sensor was validated in both in vitro and in vivo pre-clinical models and subsequently tested in a first-in-human trial. Results In the first-in-human trial, the GISMO system demonstrated feasibility, safety, and ease of use, with 66 ingestible sensors administered to 15 healthy participants. Participants reported ease in swallowing the sensors and expressed willingness to ingest multiple capsules. No device-related adverse events occurred throughout the study. GISMO is the first device capable of measuring in vivo redox balance, providing high-resolution data every 20 seconds. The data revealed consistent profiles from an oxidative environment in the stomach to a strongly reducing environment in the colon. Conclusion We successfully developed, validated, and clinically tested miniaturized technology for assessing GI health in a simple, non-invasive manner. Our ingestible sensors are the first to measure in vivo redox balance along the human gut, requiring no uncomfortable bowel preparation, and enabling real-time monitoring. This innovative technology has the potential to enable easy localization and objective quantification of inflammation, revolutionizing the diagnosis and monitoring of IBD and other gastrointestinal diseases.

Investigating the protein modification and degradation under the influence of petrol and kerosene.

During any crime scene investigation, forensic experts gather a variety of evidence in various forms, often degraded, contaminated, or fragmentary in nature. Arson-associated suicide or homicidal cases often result in partial or complete burning of this evidence, making the acquisition of crucial information more challenging. Proteins found in biological samples serve as crucial sources of evidence in criminal investigations due to their abundance within the body and greater stability than another biological macromolecule. Protein based technologies are gaining momentum for investigating wide range of forensic cases. In the present study, we probed different modifications in chicken protein subjecting after burning with petrol and kerosene individually. Structural changes and modifications in burnt chicken meat protein samples were analyzed by various biophysical techniques, such as absorption and fluorescence spectroscopy. Gel-based method such as electrophoresis was performed which showed different degradation patterns under the influence of petrol and kerosene. Our results showed that petrol-exposed meat sample caused higher rate of protein degradation than kerosene exposed samples, over a period of 12 days. Prevalent oxidative modifications, including increased carbonylation and decreased thiol levels were observed in both petrol and kerosene treated sample attributing oxidative stress environment caused by burning. Present study highlights that petrol is more potent in causing damage and protein modification than kerosene. Furthermore, this study elucidates the application of protein-based methods in forensic science, which can serve as a corroborative approach in ascertaining the cause of death in cases of burning, particularly where fuel has been utilized.

Lattice Distortions Promoting the In-Depth Reconstruction of Ni-Based Electrocatalysts with Enriched Oxygen Vacancies for the Electrochemical Oxidation of 5-Hydroxymethylfurfural toward 2,5-Furandicarboxylic Acid.

The electrocatalytic 5-hydroxymethylfurfural (HMF) oxidation reaction (HMFOR) toward 2,5-furandicarboxylic acid (FDCA) has been considered a promising approach for the substitution of the energy-consuming and hazardous oxygen evolution reaction and for the valorization of renewable biomass. However, it is limited by the susceptibility of HMF to the oxidative environment and requires efficient electrocatalysts. Herein, a NiMo complex (NiMo-N) is provided as the precatalyst for the HMFOR, exhibiting favorable performances with a current density of 450 mA·cm-2 achieved at an anodic potential of 1.4 V vs RHE (similarly hereinafter) with 50 mmol/L (mM) HMF and over 95% HMF conversion and FDCA FE for at least five cycles. Combined with quasi situ and in situ analysis, it is confirmed that the extensive lattice distortions in the precatalyst facilitate the in-depth reconstruction, increasing the accessible Ni sites and defective oxygen vacancies (Ov), which would promptly convert to high-valence Ni and active O species during the reaction. The improved performance is then attributed to the incorporation of the improved chemisorption and dehydrogenation ability of HMF by the as-evolved active sites.

Perfusate Liver Arginase 1 Levels After End-Ischemic Machine Perfusion Are Associated with Early Allograft Dysfunction.

Background/Objectives: The rising use of liver grafts from donation after circulatory death (DCD) has been enabled by advances in normothermic regional perfusion (NRP) and machine perfusion (MP) technologies. We aimed to identify predictive biomarkers in DCD grafts subjected to NRP, followed by randomization to either normothermic machine perfusion (NMP) or dual hypothermic oxygenated perfusion (D-HOPE). Methods: Among 57 DCD donors, 32 liver grafts were transplanted, and recipients were monitored for one week post-transplant. Biomarkers linked with oxidative stress, hepatic injury, mitochondrial dysfunction, inflammation, regeneration, and autophagy were measured during NRP, end-ischemic MP, and one week post-transplant. Results: Arginase-1 (ARG-1) levels were consistently higher in discarded grafts and in recipients who later developed early allograft dysfunction (EAD). Specifically, ARG-1 levels at the end of MP correlated with markers of hepatic injury. Receiver operating characteristic analysis indicated that ARG-1 at the end of MP had a good predictive accuracy for EAD (AUC = 0.713; p = 0.02). Lipid peroxidation (TBARS) elevated at the start of NRP, declined over time, with higher levels in D-HOPE than in NMP, suggesting a more oxidative environment in D-HOPE. Metabolites like flavin mononucleotide (FMN) and NADH exhibited significant disparities between perfusion types, due to differences in perfusate compositions. Inflammatory biomarkers rose during NRP and NMP but normalized post-transplantation. Regenerative markers, including osteopontin and hepatocyte growth factor, increased during NRP and NMP and normalized post-transplant. Conclusions: ARG-1 demonstrates strong potential as an early biomarker for assessing liver graft viability during perfusion, supporting timely and effective decision-making in transplantation.

7-ketocholesterol contributes to microglia-driven increases in astrocyte reactive oxygen species in Alzheimer's disease.

Oxidative stress is a prominent feature of Alzheimer's disease. Within this context, cholesterol undergoes oxidation, producing the pro-inflammatory product 7-ketocholesterol (7-KC). In this study, we observe elevated levels of 7-KC in the brains of the 3xTg mouse model of AD. To further understand the contribution of 7-KC on the oxidative environment, we developed a method to express a genetically encoded fluorescent hydrogen peroxide (H 2 O 2 ) sensor in astrocytes, the primary source of cholesterol in the brain. With this sensor, we discovered that 7-KC increases H 2 O 2 levels in astrocytes in vivo, but not when directly applied to astrocytes in vitro. Interestingly, when 7-KC was applied to a microglia cell line alone or mixed astrocyte and microglia cultures, it resulted in microglia activation and increased oxidative stress in astrocytes. Depletion of microglia from 3xTg mice resulted in reduced 7-KC in the brains of these mice. Taken together, these findings suggest that 7-KC, acting through microglia, contributes to increased astrocyte oxidative stress in AD. This study sheds light on the complex interplay between cholesterol oxidation, microglia activation, and astrocyte oxidative stress in the pathogenesis of AD.

Dual‐Release Free Iron and Breakdown of Ferroptosis Defenses to Achieve Ferroptosis Cascade Storms for Potent Antitumor Therapy

AbstractFerroptosis is a newly identified type of regulated cell death characterized by iron‐dependent lipid peroxidation. Among the main ferroptosis‐suppressing systems, the dihydroorotate dehydrogenase (DHODH)‐ ubiquinone axis is closely related to mitochondria and energy metabolism, implying that the axis protects cells from oxidative stress damage via the maintenance of redox homeostasis. However, ferroptosis initiation requires a suitable oxidative environment and a breakthrough in redox homeostatic limitations by ferroptosis‐suppressing systems. Hence, the nanoparticles are rationally engineered to achieve efficient ferroptosis induction by releasing dual‐release free iron and disrupting ferroptosis‐suppressing systems. Atovaquone (ATO)‐loaded hollow mesoporous etching zeolitic imidazolate framework‐67 double‐coated iron oxide/calcium phosphate (Fe3O4/CaP) is conjugated with polyethylene glycol. The external double‐coated Fe3O4/CaP structure enhances the efficiency of multiple reactive oxygen species (ROS) generation promoting oxidative stress. Still, it achieves free iron dual‐release to increase the content of unstable iron pools for igniting the ROS storm and lipid peroxidation spark. The release of ATO not only affects the energy metabolism of the mitochondrial respiratory chain by binding to complex III but also downregulates DHODH to restrict the ubiquinol system to disrupt the ferroptosis‐suppressing systems. Therefore, the design of this composite nanomedicine provides an approach for inducing ferroptosis and a theoretical basis for clinical ferroptosis anti‐tumor trials.

Experimental Study on Thermal Properties and Fire Risk According to Acid Value Change in Palm Oil

(1) Background: this study investigates the impact of acid value changes on the thermal degradation and fire risks of palm oil. It emphasizes the need for systematic risk management in food manufacturing and preparation processes to address safety challenges associated with high-temperature operations. (2) Methods: the study employed fire reproduction experiments, fire risk characterization tests, and thermal analyses, including differential scanning calorimetry and thermogravimetric analysis. (3) Result: higher acid values in palm oil significantly reduce smoke points, ignition points, and thermal stability, primarily due to increased free fatty acids and oxidative by-products. These effects are more pronounced in oxidative environments, highlighting the importance of controlling acid value to mitigate fire and thermal risks. (4) Conclusions: this study concludes that increased acid value in palm oil significantly reduces its thermal stability and elevates fire risks due to accelerated oxidation and thermal decomposition. It emphasizes the importance of monitoring acid value and implementing temperature control measures to enhance safety in food manufacturing and cooking processes.

Experimental study of dynamic properties of CMC flat plates in oxidative environment

Accelerated failure of CMC (Ceramic Matrix Composites) structural components in aero engines occurs under oxidative vibrational environments. This study investigates the failure mechanisms of CMCs under high-temperature oxidative vibrational conditions. Experiments were conducted to measure the vibrational response of CMC plates at 1200°C in oxygenated, non-oxygenated, and non-vibrational environments. Combined with techniques such as Energy-Dispersive X-ray Spectroscopy (EDS) and thermogravimetric analysis, the failure mechanisms of CMCs in oxidative vibrational environments were elucidated. The research results indicate that oxidation leads to a decline in the mass and mechanical properties of CMCs, resulting in a reduction in the natural frequency and response amplitude of CMC structures. The presence of vibrational loads causes the opening of matrix cracks, accelerating the oxidation of fibers within the CMC, thereby leading to a more significant decline in CMC plates’ performance and dynamic response.

Development of a multi-scale nanofiber scaffold platform for structurally and functionally replicated artificial perforating arteries.

Experimental models for exploring abnormal brain blood vessels, including ischemic stroke, are crucial in neuroscience; recently, significant attention has been paid to artificial tissues through tissue engineering. Nanofibers, although commonly used as tissue engineering scaffolds, undergo structural deformations easily, making it challenging to create uniform tissue, especially for the smallest-diameter ones such as perforating arteries. This study focused on the development of a platform capable of reconstructing structurally and functionally replicated perforating arteries. To ensure structural consistency, 3D-printed modules were developed to minimize the structural deformation of nanofibrous scaffolds when integrated into a 3D-printed vessel culture dish. Surface structures and physical characteristics of the nanofibers before and after installation were compared using scanning electron microscopy, contact angle analysis, surface area analysis, and universal testing machine (UTM) analysis. The results showed a uniform thickness distribution, topography, maximum load, tensile strain, tensile strength, surface area, pore size, and pore volume of the nanofibers. For consistency in tissue culture, smooth muscle, endothelial, and astrocyte cells were co-cultured by continuously measuring the pH of the medium and replenishing the depleted glucose using the Kalman filter control system. The functional efficacy and consistency of the artificial perforating vessels were confirmed under oxidative stress induced by exposure to hydrogen peroxide. Transcriptional mRNA expression trends were similar to those in vivo for antioxidant enzymes, neurotrophic factors, inflammatory factors, and endothelial cell activation factors, with very low variation between tissues. This study provides a research platform for studying the oxidative stress environments related to stroke by mass-producing perforating arteries with consistent structures and functions.

Constructing Bridge Hydroxyl Groups on the Ru/MOx/HZSM-5 (M = W, Mo) Catalysts to Promote the Hydrolysis Oxidation of Multicomponent VOCs.

Chlorinated and oxygenated volatile organic compounds (CVOCs and OVOCs) pose a significant threat to human health. Catalytic oxidation effectively removes these pollutants, but catalyst deactivation is a challenge. Our study focused on the hydrolysis oxidation of chlorobenzene (CB) and ethyl acetate (EA) over Ru/MOx/HZSM-5 (M = W, Mo). It was found that doping MoOx to the catalyst increased the structural hydroxyl amount and balanced surface acidity, thus significantly improving the catalytic stability, with Ru/MoOx/HZSM-5 exhibiting a better activity for CB and EA oxidation (T90% = 438 and 276 °C at space velocity = 20,000 mL g-1 h-1, respectively). Water vapor introduction considerably promoted hydrolysis oxidation and protected the active sites from being poisoned by cumulative chlorine. The synergistic interaction of the Mo-O(H)-Al structure in Ru/MoOx/HZSM-5 with the Si-OH-Al structure promotes the activation of H2O to form bridging hydroxyl groups, which provide a proton-rich environment for hydrolysis oxidation. It was also found that dissociated H2O reacted with adsorbed oxygen species to form highly active *OOH, accelerating the deep oxidation of intermediates. We believe that the present study can provide a unique strategy for the effective elimination of multicomponent VOCs under complex conditions.

Oxidative Stress and Cytoskeletal Reorganization in Hypertensive Erythrocytes.

Oxidative stress is widely recognized as a key mechanism in the development of hypertension. Under pathological conditions, such as in hypertension, oxidative stress leads to irreversible posttranslational modifications of proteins, which result in loss of protein function and cellular damage. We have previously documented physiological and morphological changes across various blood and bone marrow cell lineages, all of which exhibit elevated oxidative stress. While cytoskeletal changes in erythrocytes have been well characterized in hereditary diseases, this is the first study, to our knowledge, to investigate cytoskeletal reorganization in erythrocytes from hypertensive patients. To this end, we compared the expression patterns and subcellular distribution of key cytoskeletal proteins in erythrocytes from hypertensive individuals with those from normotensive subjects using Western blot, flow cytometry, and confocal microscopy. Our results revealed the presence of three erythrocyte subpopulations with differential expression of glycophorin A. The persistent oxidative environment in hypertensive patients causes dysregulation in the expression of glycophorin A, Band 3 protein, protein 4.1, and ankyrin, as well as the reorganization of spectrin. These alterations in protein expression and distribution suggest that oxidative stress in hypertensive individuals may induce structural modifications, ultimately impairing erythrocyte membrane elasticity and function.

GPx1 deficiency confers increased susceptibility to ferroptosis in macrophages from individuals with active Crohn’s disease

Intestinal cell death is a defining feature of Crohn’s disease (CD), a major form of inflammatory bowel disease. The focus on this aspect of enteric inflammation has mainly been on epithelial cells, while other cell types such as stromal and myeloid cells have received less attention. Hypothesising that decreased macrophage viability in an oxidative environment could be a contributing factor to the pathophysiology of CD, we found that monocyte-derived macrophages from individuals with active CD (but not those in clinical disease remission) have increased sensitivity to cell death induced by H2O2. Molecular biology and pharmacological studies ruled out apoptosis and necroptosis, while increased lipid peroxidation and surface expression of the transferrin receptor implicated ferroptosis as the mechanism of the H2O2-induced cell death: this was supported by suppression of H2O2-cytotoxicity by liproxstatin-1, a pharmacological inhibitor of ferroptosis. Selenoproteins are important antioxidants, and selenium deficiency can be a feature of CD. Despite normal dietary intake of selenium, monocyte-derived macrophages and intestinal macrophages in individuals with CD had decreased protein and/or mRNA expression of the selenoprotein, glutathione peroxidase (GPx)-1. Knockdown of GPx1 in macrophages from healthy volunteers resulted in increased H2O2-induced cell death reminiscent of that observed with macrophages from CD. In summary, monocyte-derived macrophages from individuals with CD have increased susceptibility to H2O2-induced ferroptosis cell death, that may be facilitated, at least in part, by reduced expression of the antioxidant GPx1. We suggest that reduced GPx1 in monocytes recruited to the gut and intestinal macrophages renders these cells vulnerable to reactive oxygen species-evoked ferroptosis cell death and that unraveling the participation of this pathway in Crohn’s disease may reveal novel therapeutic approaches to this chronic condition.