Impact of decontamination by plasma-activated fog (PAF) on Listeria monocytogenes mono- and mixed cultures on agar medium and foods.

Decoding the metabolic checkpoints in helminths: Opportunities for novel anthelmintic drug development.

Prolonging the anti-tumor effects of cold atmospheric plasma via exosome-mediated signaling.

Silibinin as a modulator of redox-onco axis: A natural inhibitor of oxidative damage and tumor progression.

Plasma-activated water for sustainable postharvest preservation of fruits and vegetables: mechanistic insights into physiological regulation and stress priming.

Nitric oxide and phytohormones molecular crosstalk regulating fruit quality and postharvest management.

Optimized crop management enhances sweet maize yield and reduces reactive nitrogen losses in a rainfall-uneven, water-sensitive region of Southwest China

Anthropogenic nitrogen impacts on global PM2.5-O3 co-pollution health burden.

Psoriasis is a chronic inflammatory disease characterized by thickened erythematous skin lesions covered with white and silvery scales and accompanied by macrophage infiltration into the dermis. Although 2-3% of the world's population suffers from psoriasis, there is still a requirement for novel, safe, and effective treatment options. Previously, our group demonstrated the theranostic effects of two-dimensional germanium telluride nanosheets (GeTe-NSs) in the treatment of inflammatory bowel disease. However, the precise mechanisms underlying their therapeutic action remained unclear. In this study, the specific anti-inflammatory mechanisms of GeTe-NSs in lipopolysaccharide-stimulated RAW 264.7 macrophages were evaluated, along with their therapeutic potential for psoriasis treatment in an imiquimod (IMQ)-induced murine model. GeTe-NS treatment significantly decreased cell proliferation and reduced the production of reactive nitrogen and oxygen species in activated RAW 264.7 macrophages. The GeTe-NSs lowered the mRNA levels of key pro-inflammatory mediators (Nos2, Tnf, Ccl2, and Cxcl15), while enhancing the mRNA levels of an anti-inflammatory factor (Arg1) and an antioxidant enzyme (Nqo1). Flow cytometric analysis revealed that the GeTe-NSs promoted a shift from the M1 (pro-inflammatory) macrophage phenotype toward the M2 (anti-inflammatory) phenotype. Western blot analysis demonstrated that anti-inflammatory effects were achieved by inhibiting the activation of the TLR4/CD14 and ERK/NF-kB/STAT1/STAT3 pathways. In vivo, the oral administration of GeTe-NSs in an IMQ-induced psoriasis mouse model resulted in significant improvements in clinical scores, epidermal thickening, and the proportions of M1/M2 macrophages in spleen and skin lesions. Taken together, these findings suggest that GeTe-NSs could be a promising nanomaterial for treating inflammatory diseases, including psoriasis.

Postoperative tumor management faces persistent challenges, including residual tumor survival, immune suppression, and impaired wound healing. Surgical resection eliminates the primary lesion but simultaneously removes the continuous antigen source required for sustained immune activation, leaving the postoperative microenvironment vulnerable to recurrence and metastasis. Here, a flexible wearable cold-catalytic patch is constructed by integrating thermoelectric nanorods, enzymatic components, and a zwitterionic hydrogel, enabling synergistic immune activation and enhanced tissue repair. Localized cold stimulation triggers thermoelectrocatalytic generation of reactive oxygen and nitrogen species, enabling sustained release of bioactive molecules that promote antigen presentation, amplify inflammatory cytokine secretion, and enhance immune cell infiltration. Concurrently, the thermoelectrical cues and NO signaling produced during cold catalysis stimulate fibroblast migration, angiogenesis, and extracellular matrix remodeling, thereby accelerating postoperative wound closure. In vivo studies demonstrate that this platform effectively suppresses residual tumor proliferation and distant metastasis while markedly improving healing quality. This work reports a unified thermoelectrocatalytic strategy that couples immune cascade activation with enhanced tissue repair, offering a broadly applicable paradigm for next-generation postoperative tumor therapy.

Engineered nanoparticles (ENPs) are increasingly recognized as promising tools for modulating plant stress responses; however, their underlying mechanisms and associated risks remain under debate. This review integrates recent advances showing that ENPs can reprogram plant redox homeostasis through multiple pathways, including direct surface redox activity, nanozyme-like catalysis, ion release, and disruption of organellar electron transport. In addition, ENPs influence membrane physicochemical properties, transcriptional regulation, metabolic fluxes, hormonal crosstalk, epigenetic modifications, and the structure of the plant-associated microbiome. These processes produce distinct reactive oxygen and nitrogen species (ROS/RNS) signatures that activate Ca2+ fluxes, mitogen-activated protein kinase (MAPK) cascades, and downstream transcriptional networks. We emphasize the importance of dose-dependent-often hormetic-responses, the critical role of the rhizosphere microbiome, and the application of spatially resolved techniques (e.g., μ-XRF, NanoSIMS, and spatial omics) to link NP fate with localized redox dynamics. Finally, we propose a safe-by-design framework that incorporates standardized NP characterization, appropriate ionic and inert controls, and predictive modeling approaches. This framework aims to facilitate the risk-informed and sustainable deployment of ENPs in agriculture.

Reactive species as regulators of immune cell metabolism, tolerance, and autoimmunity.

UVC irradiation is widely used for disinfection, yet its efficacy is sometimes compromised by bacterial photoreactivation and dark repair. This study demonstrates that pre-exposure to UVA irradiation in the presence of environmentally relevant nitrite (NO2-) significantly suppresses both repair pathways during subsequent UVC treatment. At 1.0 mg-N L-1 NO2- and 612 mJ cm-2 UVA, sequential (UVA-UVC)/NO2- treatment reduced photoreactivation and dark repair to less than 6% and 3%, respectively. This inhibition was consistent across four representative waterborne bacteria, including Gram-negative (E. coli and A. hydrophila) and Gram-positive (S. aureus and B. subtilis) strains, and remained effective in aquaculture tailwater and municipal secondary effluent (indigenous NO2- ≤ 0.3 mg-N L-1). Single-species dominant systems identified ONOO-/HOONO and NO2•, rather than HO• or NO•, as the primary mediators of repair suppression. Mechanistic investigations revealed that low-dose RNS did not cause nonspecific structural damage but instead selectively disrupted ATP biosynthesis by targeting key tricarboxylic acid cycle enzymes, including isocitrate dehydrogenase and citrate synthase. Resulting ATP depletion reduced transcription of recA, phr, and other repair-related genes, preventing activation of the bacterial repair machinery. This work provides a sustainable, low-dose, and highly targeted method to overcome bacterial repair and improve UVC disinfection efficiency.

Following ultraviolet (UV) excitation, nitroaromatic molecules can undergo complex excited-state relaxation and photofragmentation processes that may generate reactive nitrogen oxide species (NOx). However, the excited-state dynamics associated with NOx formation remain incompletely understood. Here, we investigate the photochemistry of nitrobenzene using time-resolved X-ray absorption spectroscopy at the oxygen K-edge, combined with high-level electronic structure calculations. Upon 267 nm excitation in the gas phase, nitrobenzene undergoes rapid relaxation from the initially populated 1(LBππ*) state to the 1(nAπ*)/3(nAπ*) states, where a significant fraction of the population remains trapped for at least 100 ps rather than undergoing rapid internal conversion to the S0 state. Signatures of NO or NO2 formation are not observed within this time window at the current signal-to-noise ratio, indicating that photofragmentation remains a minor channel up to 100 ps. These results provide element-specific insight into nitroaromatic photochemistry and support a mechanism in which photofragmentation is delayed by transient excited-state trapping.

Reactive nitrogen (Nr) species serve as a pivotal catalytic engine in tropospheric oxidation processes. Furthermore, their multiphase transport and interfacial conversions can also perturb biogeochemical equilibria across marine, terrestrial, and atmospheric systems. This review integrates groundbreaking advances in the cycling and conversion of Nr at multimedia surfaces (gas-aqueous, gas-particle, and gas-soil interfaces), revealing their key role in driving the formation of atmospheric fine particulate matter and enhancing atmospheric oxidizing capacity. The critical environmental factors affecting the cycle at each active interface were also systematically investigated and comprehensively analyzed. By integrating laboratory studies, field campaigns, and modeling simulations, we reveal how aerosol-mediated Nr-S chemistry creates self-amplifying positive feedback that exacerbates haze formation. These mechanisms partly explain why the advanced model often underestimates sulfate concentrations in megacities, providing direct support for pollution control strategies. Our analysis bridges molecular-scale interfacial processes with the fast increase in regional fine particles, offering actionable insights for scientists, policymakers, and engineers combating atmospheric complex pollution, particularly in developing countries.

Upon activation, macrophages generate substantial levels of reactive nitrogen species, which can induce alkylating damage in the DNA of intracellular Mycobacterium tuberculosis (Mtb) and thereby restrict bacterial replication. However, the molecular mechanisms by which Mtb repairs such DNA lesions remain poorly understood. Here, we identified genes required for Mtb survival in distinct macrophage subsets using transposon insertion sequencing. Among these, tagA displayed a specialized role in Mtb survival in M1-polarized macrophages, as well as in mice at 4 wk postinfection, a stage when macrophages are biased toward an M1-polarized state. Mechanistically, TagA conferred resistance to the DNA alkylating agent methyl methanesulfonate through its 3-methyladenine (3-MA) excision activity with Glu48 serving as a key catalytic residue for substrate binding. Critically, TagA was found to protect the Mtb genome from alkylation damage caused by nitrosative stress-a hallmark of the M1-polarized macrophage microenvironment. Furthermore, pharmacological inhibition of inducible nitric oxide synthase (iNOS) with S-methylisothiourea sulfate in mice or genetic deletion of nos2a in zebrafish markedly rescued the survival defect of ΔtagA. Together, these findings reveal a previously unappreciated mechanism by which the DNA repair enzyme TagA protects Mtb against 3-MA DNA damage under nitrosative stress, thereby promoting bacterial survival in M1-polarized macrophages and during in vivo infection.

Organic nitrate esters (R-ONO2) are structurally and electronically distinct from nitro compounds, featuring a polarized C-O-NO2 linkage with an intrinsically weak O-N bond. This characteristic imparts unique reactivity, enabling controlled bond cleavage and rendering nitrate esters valuable in energetic materials, pharmaceuticals (as nitric oxide (NO) donors), and as synthetic intermediates. Nitrooxylation, the installation of the -ONO2 group, has historically relied on harsh mixed-acid systems (e.g., nitric acid/sulfuric acid), which suffer from poor selectivity, limited functional-group tolerance, and significant safety concerns. Recent advances have shifted the field toward milder and more controlled approaches. Catalytic systems, bench-stable nitrooxy transfer reagents, and alternative activation modes have improved selectivity and operational safety. In particular, photochemical, electrochemical, and mechanochemical strategies enable the in situ generation of reactive nitrogen oxide species (e.g., NO2•, NO3•) under controlled conditions, expanding the scope to include alkene difunctionalization, C(sp3)-H functionalization, and selective O-nitration of alcohols. This review provides a comprehensive overview of the evolution of nitrooxylation chemistry, from classical methods to modern synthetic platforms. Emphasis is placed on mechanistic understanding, reagent design, and the interplay between electronic structure and reactivity, with the aim of guiding future developments toward safe, selective, and sustainable nitrate ester synthesis.

Physical plasma for lignin valorization: comprehensive analysis of aromatic substances derived from cleavage and synthesis reactions using guaiacylglycerol-β-guaiacyl ether as model compound.

Inflammatory bowel disease (IBD) is a relapsing gastrointestinal disorder depicted by persistent oxidative/nitrosative stress, mucosal barrier disruption, and maladaptive immune activation. Herein, we report that sulfasalazine- and cerium ion-loaded polymersomes (SSZ/Ce-Some) that effectively treat IBD through superior capability of scavenging reactive oxygen and nitrogen species (RONS) and promotion of colonic mucosal repair. SSZ/Ce-Some exhibits potent superoxide dismutase (SOD)-like and catalase (CAT)-like catalytic activities, efficiently scavenges representative ROS, and markedly generates oxygen. Its excellent neutralization of RNS (NO) together with superoxide indicates inhibition of tissue-destructive peroxynitrite. SSZ/Ce-Some inhibits inflammatory macrophages and dendritic cell activation and suppresses pro-inflammatory cytokine secretion. In acute colitis, SSZ/Ce-Some accumulates in inflamed colons, alleviates intestinal inflammation, and preserves epithelial tight junction integrity. Moreover, oral SSZ/Ce-Some in a mucoadhesive hydrogel safely and effectively treats chronic Crohn's disease, with tissue repair and immune regulation. Overall, SSZ/Ce-Some with superior RONS-detoxifying capacity represents a promising therapeutic strategy for IBD treatment.

NIR chemosensor for rapid tracking and evaluating hypochlorous acid level within biosystem and inflammatory DILI models.