Search Results (1,996)

This study presents a quantitative simulation analysis of hydrogen-enriched methane (HENG) storage with nitrogen as the cushion-gas in a depleted gas reservoir by varying three key operational parameters: the injection/withdrawal period, hydrogen blending ratio (5–20%), and injection depth. Ten injection–withdrawal cycles were modeled for each scenario, and performance was evaluated using cycle-averaged and cumulative hydrogen purity, recovery factors, and the mixing zone size. Extending the injection period increased hydrogen purity to 20.00–20.26% and reduced nitrogen to 0.001–0.003%, but recovery decreased from 65.63 to 53.83–41.09% due to enhanced dispersion and residual trapping. The blending ratio was the dominant control: 20% blending yielded 19.9–20.0% purity with nitrogen as low as 0.00–0.03%, whereas 5–10% blending produced lower purity but minimized nitrogen production to 0.97–1.08%. Injection depth affected nitrogen recovery more than purity, increasing from 0.72–1.20% (upper) to 1.46–1.61% (lower), along with thicker mixing zones. Final mixing zone size ranged from 3176 to 5546 blocks, with smaller zones consistently linked to higher purity and lower nitrogen breakthrough. The shut-in period further reduced nitrogen recovery from 6.49 to 1.33% and stabilized mixing behavior. Overall, minimizing late-cycle mixing zone thickness is essential for maintaining HENG storage performance. Although this study provides quantitative insights into HENG operational strategies, the use of a homogeneous grid and simplified fluid properties limits representation of geological heterogeneity and reactive processes. Future work will incorporate heterogeneity and reaction modeling into field-scale simulations to validate and refine these operating strategies for practical deployment. Full article

The energy transition in the transportation sector makes hydrogen a promising candidate as a fuel for internal combustion engines; however, its tendency to knock limits its use to lean mixtures, resulting in a reduction in performance. In this context, water injection represents a technical solution capable of reducing both the risk of knocking and the pollutant emissions of nitrogen oxide (NOx). Although several studies have been published on the benefits of water injection, its capacity to suppress high-intensity knocking phenomena was never investigated and is not traceable in the scientific literature. On account of this lack, the authors of the present paper experimentally evaluate the effectiveness of port water injection in suppressing high-intensity knock phenomena and its potential in terms of nitrogen oxide emission reduction. Differently from previous works, a highly reactive fuel (PRF60) was adopted to reproduce, as closely as possible, the knocking tendency of hydrogen. The tests were carried out on a single-cylinder CFR engine, suitably modified to allow port water injection, operating with stoichiometric air–fuel mixture (λ = 1) and at low engine speed, which constitutes the most critical condition, since it allows for heavy knocking and is less favorable for injected water evaporation. Moreover, aiming to assess the effect of spray atomization, the tests were repeated using three different water injection pressure levels. The study presented, however, is confined to the effects of port water injection on knock suppression and NOx emission reduction, while no engine performance or efficiency variation were considered. The results showed that port water injection, with water addition up to 40% by mass with respect to fuel, enables an almost complete suppression of high-intensity knocking phenomena, along with a significant reduction in NOx emissions (up to −62%). Full article

Ozone (O₃) is a reactive oxidant increasingly applied in biomedical settings, yet its dose-dependent effects on innate immune cells, particularly those from non-human species, remain insufficiently defined. Within a One Health framework, this study examined how two clinically relevant O₃ exposure regimens (30 µg/mL and 90 µg/mL) affect porcine neutrophils and monocytes isolated from peripheral blood. Cell viability, reactive oxygen and nitrogen species (RONS) production, and the activity of key enzymes (myeloperoxidase, elastase, alkaline phosphatase, arginase) were assessed at 1 h and 24 h post-exposure. The lower dose induced mild functional activation without compromising viability, whereas the higher dose triggered pronounced oxidative stress, enhanced degranulation, and reduced neutrophil viability by more than 60%. Neutrophils exhibited a stronger and more dynamic response than monocytes, which retained viability and differentiation capacity at 30 µg/mL but showed impaired function at 90 µg/mL. These findings highlight the dual nature of O₃, where controlled exposure may support immunomodulation, while excessive dosing disrupts cell function. Defining safe and effective therapeutic windows remains critical for future applications. Full article

Per- and polyfluoroalkyl substances (PFAS) are emerging contaminants that persist in soil environments, necessitating reliable models to predict their fate and transport. This study evaluates the performance of three theoretical models in estimating the maximum adsorption capacity (Qmax) of perfluorooctanoic acid (PFOA) on kaolinite and montmorillonite clay minerals. The models assessed include a van der Waals interaction-based approach, a monolayer adsorption capacity model, and a surface site density model emphasizing reactive hydroxyl groups at mineral edges. Benzene, nitrogen, and glyphosate molecules were used as reference compounds for model validation. Results indicated that the van der Waals model significantly underestimated Qmax (0.0007 mg·g⁻¹ for kaolinite), while the monolayer capacity model produced substantial overestimations (17.51 mg·g⁻¹) compared to the experimental range (0.10–10.0 mg·g⁻¹). The surface site density model provided the most accurate predictions (3.39 mg·g⁻¹ for kaolinite), although it slightly underestimated values for montmorillonite (0.20 mg·g⁻¹) by excluding interlayer adsorption. These discrepancies demonstrate that simplified models cannot adequately capture the complex adsorption behavior of PFAS. Accurate prediction requires site-specific approaches incorporating electrostatic forces, hydrogen bonding, and steric effects. As PFAS accumulation in soil directly contributes to groundwater contamination, improving adsorption models is essential for accurate risk assessment and the development of effective remediation strategies. Full article

Background: Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a multifactorial liver disease in which mitochondrial dysfunction, oxidative stress, and inflammation play key roles in driving the progression toward metabolic dysfunction-associated steatohepatitis (MASH) and hepatocellular carcinoma (HCC). Dysfunctional mitochondria generate excess reactive oxygen species (ROS), impair antioxidant defenses, activate pro-inflammatory pathways and hepatic stellate cells, and perpetuate liver injury. Mitochondrial Complex I is a major ROS source, particularly under conditions of dysregulated energy metabolism. Since Complex I inhibition by metformin was shown to reduce ROS and activate the adenosine monophosphate-activated protein kinase (AMPK), this study aimed to evaluate whether a novel Complex I Modulator (CIM, BI4500) could attenuate oxidative stress, inflammation, and consequently reduce lipid accumulation and fibrosis in a methionine- and choline-deficient diet (MCD)-fed rat model of MASH. Methods: Rats were fed an MCD or an isocaloric control diet for six weeks. From week four, animals received daily oral treatment with CIM (10 mg/kg) or vehicle (Natrosol). At the endpoint, liver tissue was collected for histological, biochemical, and molecular analyses. Lipid droplet area, inflammatory infiltration, and collagen deposition were evaluated on tissue sections; total lipid content and oxidative stress markers were assessed in homogenates and isolated mitochondria. Molecular pathways related to oxidative stress, lipid metabolism, and fibrosis were assessed at protein and mRNA levels. Results: CIM treatment significantly reduced oxidative stress (ROS, lipid peroxidation, nitrogen species), promoting AMPK activation and metabolic reprogramming. This included increased expression of peroxisome proliferator-activated receptor alpha (PPAR-α) and its target genes, and decreased sterol regulatory element binding protein-1c (SREBP-1c)-driven lipogenesis. These changes halted fibrosis progression, as confirmed by Picro-Sirius Red staining and fibrosis markers. Conclusions: these findings indicate that Complex I modulation may represent a promising strategy to counteract MASLD progression toward MASH. Full article

Microplastics (MPs) have emerged as persistent environmental pollutants with adverse effects on ecosystems and human health. Conventional removal methods, such as filtration and sedimentation, primarily rely on physical separation without addressing the degradation of MPs, leading to their accumulation and the risk of secondary pollution. This review explores the potential of advanced oxidation processes (AOPs), including photocatalysis, electrochemical oxidation, Fenton processes, sulfate radical-based oxidation, sonochemical treatment, ozonation, and plasma technologies, which generate reactive oxygen and nitrogen species capable of promoting polymer chain scission, microbial biodegradation, and the oxidative fragmentation and mineralization of MPs into non-toxic byproducts. Hybrid AOP systems combined with biological treatments or membrane-based filtration are also examined for their effectiveness in degrading MPs, as well as for scalability and the environmental impacts of their byproducts when integrated into existing wastewater treatment systems. The review further discusses challenges related to operational parameters, energy consumption, and the formation of secondary pollutants. By identifying current knowledge gaps and future research directions, this review provides insights into optimizing AOPs and integrations of AOPs with biological treatments or membrane-based processes for sustainable MP remediation and water treatment applications. Full article

To reveal the driving mechanisms of oxidative carbon components in urban forest soils in highly urbanized areas, this study collected 126 soil samples from the 0–30 cm layer of typical urban forests in Shenzhen, China. Soil organic carbon (SOC) was classified into four fractions based on oxidation stability: highly oxidizable organic carbon (VAC), moderately oxidizable organic carbon (AC), poorly oxidizable organic carbon (PAC), and inert oxidizable organic carbon (IAC). Integrating multi-source data on climate, topography, vegetation, soil, and urbanization, we adopted a synergistic multi-model approach to screen key drivers, identify nonlinear thresholds, and quantify pathway contributions, thereby systematically exploring the dominant characteristics and driving mechanisms of soil carbon components under urbanization. The results showed that (1) urban forest soils in Shenzhen were dominated by reactive carbon, with VAC accounting for the highest proportion of SOC, and the proportion of reactive organic carbon was significantly higher than that of recalcitrant organic carbon; (2) SOC and total nitrogen (TN) were the core driving factors of carbon fractions, and the number of regulatory factors increased with the enhancement of carbon fraction oxidation stability; (3) soil factors directly affected carbon fractions, while urbanization indirectly acted on inert carbon by altering vegetation characteristics. Based on the research results, urban soil and forest managers can implement zonal management for carbon fractions with different oxidation stabilities, which is expected to effectively enhance the carbon sink capacity and stability of urban forest soil carbon pools, providing practical support for ecological sustainable development. Full article

Uric acid (UA), a key end-product of human purine metabolism, serves as an important biomarker linked to multiple disorders. This study developed a novel enzyme-free colorimetric sensing platform based on starch-derived nitrogen-doped biochar (NC) for the highly sensitive and selective detection of UA in human body fluids. The NC material with a high specific surface area and abundant nitrogen active sites was prepared via a two-step strategy involving hydrothermal synthesis followed by high-temperature pyrolysis, using starch and urea as raw materials. Under mild conditions, the NC effectively catalyzes dissolved oxygen to produce reactive oxygen species (·O₂⁻ and ¹O₂), which oxidize 3,3′,5,5′-tetramethylbenzidine (TMB) to a blue-colored oxidation product (TMBox). The presence of UA reduces TMBox to colorless TMB, leading to a measurable decrease in absorbance at 652 nm and enabling quantitative UA detection. Key reaction conditions were systematically optimized. Material characterization and mechanistic investigations confirmed the catalytic performance of the NC. The method demonstrated a wide linear response from 10 to 500 μmol·L⁻¹, with a detection limit of 4.87 μmol·L⁻¹, and demonstrated outstanding selectivity, stability, and reproducibility. Practical application in human serum and urine samples yielded results consistent with clinical reference ranges, and spike-recovery rates ranged from 95.5% to 103.6%, indicating great potential for real-sample analysis. Full article

This narrative review aims to systematize the current knowledge on the dual role of reactive oxygen species and reactive nitrogen species in cancer processes, from their physiological function in redox signaling to their pathological impact in oxidative distress. The mechanisms of biomolecule damage, particularly DNA, and deregulation of signaling pathways induced by excessive ROS/RNS concentrations, which promote neoplastic transformation, are presented. The importance of diet and endogenous antioxidants in cancer prevention is also discussed, emphasizing the role of natural antioxidants in prevention and adjunctive therapy. In this context, oleanolic acid emerges as a promising compound with dual action modulating oxidative stress, capable of balancing cellular redox responses. We discuss the most important antioxidant mechanisms of oleanolic acid, the interconnection of oxidative stress with carcinogenesis-related pathways, anticancer mechanisms mediated by oxidative stress modulation, and structural modifications and modern application techniques that improve its bioavailability, as well as future perspectives on oleanolic acid research in the context of its antioxidant and anticancer activity. Overall, available experimental and preclinical data indicate that oleanolic acid, through pleiotropic modulation of oxidative stress and signaling networks, holds promise as an adjuvant agent in cancer prevention and therapy. Full article

Melatonin, an ancient and evolutionarily conserved indolamine, has long attracted attention for its multifunctional roles in redox homeostasis. More recently, it has been studied in relation to immune regulation and cancer biology. Beyond its well-known circadian function, melatonin modulates oxidative stress by directly scavenging reactive oxygen and nitrogen species and by upregulating antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. At the same time, it exerts wide-ranging immunomodulatory functions by influencing both innate and adaptive immune responses. All these actions converge within the tumor microenvironment, where oxidative stress and immune suppression drive cancer progression. Although the antitumoral effects of melatonin have traditionally been interpreted through its actions on T cells and NK cells, recent studies identify macrophages as an underappreciated and pivotal target. Notably, melatonin influences macrophage polarization, favoring antitumor M1 phenotypes over pro-tumoral M2 states, while attenuating chronic inflammation and restoring mitochondrial function. This review summarizes current knowledge on melatonin’s antioxidant and immunoregulatory mechanisms, highlighting its impact on the tumor immune microenvironment, with a particular focus on the growing recognition of macrophages as a compelling new axis through which melatonin may exert anticancer effects. Full article

Salinity shock severely impairs the partial denitrification/anammox (PD/A) process, leading to prolonged functional deterioration and slow reactivation of anaerobic ammonium-oxidizing bacteria (anammox). To develop an effective strategy for mitigating salinity-induced inhibition, this study systematically examined the role of exogenous hydroxylamine (NH₂OH) in accelerating PD/A recovery using short-term batch assays and long-term reactor operation. Hydroxylamine exhibited a clear concentration-dependent effect on system reactivation. In batch tests, low-dose hydroxylamine (10 mg/L) markedly enhanced anammox activity, increasing the ammonium oxidation rate to 5.5 mg N/(g VSS·h), representing a 42.5% increase, indicating its potential to stimulate key nitrogen-transforming pathways following salinity stress. During continuous operation, hydroxylamine at 5 mg/L proved optimal for restoring reactor performance, achieving stable nitrogen removal with 87% NH₄⁺-N removal efficiency. The nitrite transformation ratio (NTR) reached approximately 80% within 13 cycles, 46 cycles ahead of the control, while simultaneously promoting the enrichment of key functional microbial taxa, including Thauera and Candidatus Brocadia. Hydroxylamine addition also triggered the production of tyrosine- and tryptophan-like proteins within extracellular polymeric substances, which enhanced protective and metabolic functionality during recovery. In contrast, a higher hydroxylamine dosage (10 mg/L) resulted in persistent NO₂⁻-N accumulation, substantial suppression of Candidatus Brocadia (declining from 0.67% to 0.09%), and impaired system stability, highlighting a dose-sensitive threshold between stimulation and inhibition. Overall, this study demonstrates that controlled low-level hydroxylamine supplementation can effectively reactivate salinity-inhibited PD/A systems by enhancing nitrogen conversion, reshaping functional microbial communities, and reinforcing stress-response mechanisms. These findings provide mechanistic insight and practical guidance for improving the resilience and engineering application of PD/A processes treating saline wastewater. Full article

This study presents the development of a smart packaging material utilizing garlic-derived nitrogen-doped carbon dots (CDs) integrated into a whey protein–starch (WP-S) emulsion. The research aimed to create a real-time, non-invasive biosensor capable of detecting microbial spoilage. The synthesized CDs demonstrated strong pH-sensitive photoluminescence, exhibiting distinct changes in CIE coordinates and fluorescence intensity in response to varying pH values. The WP-S-CDs emulsion was tested against E. coli, S. aureus, and C. albicans. The results showed that the composite film provided a clear colorimetric shift and fluorescence quenching, both of which are directly correlated with microbial metabolic activity. The physical and electronic properties of the composite were investigated to understand the sensing mechanism. Scanning electron microscopy (SEM) of the dried film revealed that the WP-S-CDs system formed a more porous structure with larger pore sizes (3.63–8.18 µm) compared to the control WP-S film (1.62–6.52 µm), which facilitated the rapid diffusion of microbial metabolites. Additionally, density functional theory (DFT) calculations demonstrated that the incorporation of CDs significantly enhanced the composite’s electronic properties by reducing its band gap and increasing its dipole moment, thereby heightening its reactivity and sensitivity to spoilage byproducts. In a practical application on apples, the WP-S-CDs coating produced a visible red spot, confirming its function as a dynamic sensor. The material also showed a dual-action antimicrobial effect, synergistically inhibiting C. albicans while exhibiting an antagonistic effect against bacteria. These findings validate the potential of the WP-S-CDs emulsion as a powerful, multi-faceted intelligent packaging system for food quality monitoring. Full article

Peroxynitrite (ONOOH/ONOO⁻) is increasingly recognized as a key intermediate in advanced oxidation processes (AOPs), yet its role in water treatment remains insufficiently defined. This study provides mechanistic insights into peroxynitrite-mediated AOPs through competition kinetics method, demonstrating that both decomposition and pollutant degradation are strongly pH-dependent, with ONOOH dominating stability and radical pathways across pH 5.0−9.0, while its decay rate decreases from 1.2 s⁻¹ to 0.0022 s⁻¹. The interplay of HO^• and diverse reactive nitrogen species (RNS, including reactive nitrogen radicals and peroxynitrite) dictates pollutant-specific degradation efficiencies, with RNS showing a unique reliance in degrading bisphenol A—contributing up to 66.7% at pH 8.0. Buffer chemistry further modulates these pathways: bicarbonate accelerates peroxynitrite decay via CO₂ and CO₃^•−-mediated acceleration (resulting in a 361.9% increase at pH 9.0), while borate promotes reactive nitrogen radical formation but suppresses HO^• contributions. Importantly, peroxynitrite was shown to facilitate N-nitrosodimethylamine formation in the presence of dimethylamine, with yields maximized under alkaline conditions and attenuated by bicarbonate. These quantitative findings underscore the critical roles of pH and buffer chemistry in optimizing peroxynitrite-based water treatment while mitigating byproduct risks. Full article

Phosphate is emerging as an active mediator of oxidative stress and vascular injury in chronic kidney disease (CKD). This emerging pathophysiological framework, referred to as “Phosphatopathy”, describes the systemic syndrome driven by chronic phosphate overload and characterized by oxidative stress, inflammation, endothelial dysfunction, vascular calcification, cellular senescence, and metabolic imbalance. Beyond being a biochemical marker, phosphate overload triggers NOX-derived reactive oxygen species (ROS), activates Wnt/β-catenin and TGF-β signaling, and disrupts the FGF23–Klotho axis, promoting endothelial dysfunction, vascular calcification, and left ventricular hypertrophy (LVH). These pathways converge with systemic inflammation and energy imbalance, contributing to the malnutrition–inflammation–atherosclerosis (MIA) syndrome. Experimental and clinical data reveal that the phosphate/urinary urea nitrogen (P/UUN) ratio is a sensitive biomarker of inorganic phosphate load, while emerging regulators such as microRNA-125b and calciprotein particles integrate phosphate-driven oxidative and inflammatory responses. Therapeutic strategies targeting phosphate burden—rather than serum phosphate alone—include dietary restriction of inorganic phosphate, non-calcium binders, magnesium and zinc supplementation, and activation of important pathways related to the activation of antioxidant defense such as AMP-activated protein kinase (AMPK) and SIRT1. This integrative framework redefines phosphate as a modifiable upstream trigger of oxidative and metabolic stress in CKD. Controlling phosphate load and redox imbalance emerges as a convergent strategy to prevent vascular calcification, improve arterial stiffness, and reduce cardiovascular risk through personalized, mechanism-based interventions. Full article

We aimed to investigate the association between oxidative stress (OS), inflammation, and kidney function and the predictive ability of OS for mortality and cardiovascular disease in 143 patients with type 2 diabetes (T2DM) and various degrees of kidney function. At baseline, we assessed catalase, nitrogen oxides (NOx), malondialdehyde (MDA), advanced oxidation products (AOPPs), myeloperoxidase (MPO)], kidney function, and C-reactive protein (CRP). All patients were followed for 57 months, with the combined primary outcome of death/cardiovascular (CV) event, whichever occurred first. NOx was an independent predictor of estimated glomerular filtration rate (B = −0.097, p = 0.006), and MPO was correlated with glycated hemoglobin (r = 0.17, p = 0.046), CRP (r = −0.18, p = 0.032), and serum albumin (r = 0.2, p = 0.011, Spearman’s rho). During the follow-up, 24 composite events were documented. Kaplan–Meier curves showed that smoking (p = 0.029), serum albumin (p = 0.014), and MPO (p = 0.024, log-rank test) were associated with the outcome. In multivariate Cox regression models, smoking and MPO were independent predictors of the composite outcome (hazard ratio—HR = 2.8, p = 0.004, 955 confidence interval—CI 1.05–7.5 and HR = 0.99, p = 0.015, 95% CI: 0.98–1.00, respectively), after adjustment for several cofactors. OS might be associated with CV disease in T2DM. Full article