Production Of Nitrogen Species Research Articles

A hierarchal model for bacterial cell inactivation in solution by direct and indirect treatment using cold atmospheric plasmas

Cold atmospheric plasma devices have shown promise for a variety of plasma medical applications, including wound healing and bacterial inactivation often performed in liquids. In the latter application, plasma-produced reactive oxygen and nitrogen species (RONS) interact with and damage bacterial cells, though the exact mechanism by which cell damage occurs is unclear. Computational models can help elucidate relationships between plasma-produced RONS and cell killing by enabling direct comparison between dissimilar plasma devices and by examining the effects of changing operating parameters in these devices. In biological applications, computational models of plasma-liquid interactions would be most effective in design and optimization of plasma devices if there is a corresponding prediction of the biological outcome. In this work, we propose a hierarchal model for planktonic bacterial cell inactivation by plasma produced RONS in liquid. A previously developed reaction mechanism for plasma induced modification of cysteine was extended to provide a basis for cell killing by plasma-produced RONS. Results from the model are compared to literature values to provide proof of concept. Differences in time to bacterial inactivation as a function of plasma operating parameters including gas composition and plasma source configuration are discussed. Results indicate that optimizing gas-phase reactive nitrogen species production may be key in the design of plasma devices for disinfection.

Effect of agitation speed on methylene blue discoloration kinetics via ambient air cold plasma

AbstractThis research investigates the kinetics of methylene blue (MB) discoloration using ambient air cold plasma, with a focus on the impact of agitation speed (100 and 750 rpm). The study revealed pseudo‐first‐order kinetics for MB discoloration, pinpointing optimal conditions at 35.00°C and 100 rpm. These parameters minimized half‐life times, correlated with observed kobs values. A decreasing pH trend, more pronounced at 750 rpm, was attributed to increased acidic nitrogen species (HNO3 and HNO2) production, adversely affecting dye discoloration. Concurrently, enhanced electrolyte concentration was noted from rising conductivity due to plasma production of reactive species followed by solubilization in the aqueous phase. The calculated thermodynamic activation parameters comprised: Ea = 7.96 kJ mol−1, ΔH‡ = +5.53 kJ mol−1, ΔS‡ = −253.23 J K−1 mol−1, and ΔG‡ = +79.77 kJ mol−1 (100 rpm); and Ea = 12.94 kJ mol−1, ΔH‡ = +13.78 kJ mol−1, ΔS‡ = −239.06 J K−1 mol−1, and ΔG‡ = +80.58 kJ mol−1, (750 rpm). The lowest Ea and ΔG‡ values at 100 rpm reinforced lower agitation favoring the reaction. The study demonstrated a linear decay of the reaction rate constant with the square root of ionic strength. This result, besides the negative activation entropy and moderate activation enthalpy led to a proposition to the determinant step for the transition state formation, involving an associative step between a solvated electron and the protonated substrate. The optimal dye discoloration rate and energy yield were observed at 35.00°C and 100 rpm, with values of 97.2% and 3.371 × 10−2 g kW−1 h−1, respectively.

Biocompatible cdots dual role: Nanophotosensitizers for hypoxic photodynamic therapy and scavenging nanozyme biosensing

Within this study we report a non-toxic nanomaterial suitable for Photodynamic Therapy (PDT) under hypoxic conditions. PDT relies on the production of reactive oxygen and nitrogen species that can lead to cancer cells death. Currently, PDT is limited by: the development of efficient photosensitizers that can produce these radicals in situ; and the oxygen level requirement. The produced Carbon Dots (Cdots) successfully destroy human melanoma cancer cells upon 5 min irradiation using 450 nm wavelength due to the in situ production of NO•. As such, this nanophotosensitizer is applicable regardless of the cells molecular oxygen levels. Additionally, this nanomaterial acts as a scavenging nanozyme biosensor allowing to follow-up, in situ, the released NO• concentration, thereby offering a tight control over the NO• concentration in real-time and, its maintenance within the therapeutic window. Hence, this work offers a novel theranostic and NO• scavenging nanozyme biosensing nanoplatform that allows high control for hypoxic-PDT cancer application even in low doses and with 5 min irradiation.

Evaluation of genotoxic damage, production reactive oxygen and nitrogen species in Plasmodium yoelii yoelii exposed to sodium metavanadate

Malaria represents the greatest global health burden among all parasitic diseases, with drug resistance representing the primary obstacle to control efforts. Sodium metavanadate (NaVO3) exhibits antimalarial activity against the Plasmodium yoelii yoelii (Pyy), yet its precise antimalarial mechanism remains elusive. This study aimed to assess the antimalarial potential of NaVO3, evaluate its genotoxicity, and determine the production of reactive oxygen and nitrogen species (ROS/RNS) in Pyy. CD-1 mice were infected and divided into two groups: one treated orally with NaVO3 (10 mg/kg/day for 4 days) and the other untreated. A 50% decrease in parasitemia was observed in treated mice. All experimental days demonstrated DNA damage in exposed parasites, along with an increase in ROS and RNS on the fifth day, suggesting a possible parasitostatic effect. The results indicate that DNA is a target of NaVO3, but further studies are necessary to fully elucidate the mechanisms underlying its antimalarial activity.

Glycated LDL generates reactive species that damage cell components, oxidize hemoglobin and alter surface morphology in human erythrocytes

Low-density lipoprotein (LDL) transports cholesterol to various tissues via the blood. Glycation of LDL occurs during hyperglycemic condition which is characterised by persistently high blood glucose level. Circulating erythrocytes can come in direct contact with glycated LDL (G-LDL). The objective of this study was to investigate the effect of G-LDL on human erythrocytes, specifically on hemoglobin, intracellular generation of reactive species and the antioxidant defence system. Isolated erythrocytes were incubated with G-LDL (3 and 6 mg/ml) and native LDL (6 mg/ml) at 37 °C for 24 h. Native LDL and G-LDL untreated erythrocytes were similarly incubated at 37 °C and served as control. G-LDL treatment increased hemolysis compared to control and native LDL-treated erythrocytes. Incubation of erythrocytes with G-LDL led to an increase in protein oxidation and lipid peroxidation while greatly decreasing the total sulfhydryl content. It also significantly enhanced hemoglobin oxidation, heme degradation, and the release of free iron moiety. Treatment with G-LDL led to an appreciable increase in the production of reactive oxygen and nitrogen species. The antioxidant power and activities of major antioxidant enzymes were drastically reduced, while critical membrane-bound enzymes were inhibited. The surface morphology of G-LDL-treated erythrocytes was altered leading to the formation of echinocytes. Importantly, treatment of erythrocytes with native LDL did not significantly affect the above-mentioned parameters and values were similar to the corresponding controls. Thus, G-LDL is cytotoxic to human erythrocytes and causes oxidative damage to cell components. This can reduce the oxygen-transporting ability of blood and also result in red cell senescence and anemia.

Evaluation of degradation efficacy and toxicity mitigation for 4-nitrophenol using argon and air-mixed argon plasma jets

This paper investigates the effects of argon (Ar) and that of Ar mixed with ambient air (Ar–Air) cold plasma jets (CPJs) on 4-nitrophenol (4-NP) degradation using low input power. The introduction of ambient air into the Ar-Air plasma jet enhances ionization-driven processes during high-voltage discharge by utilizing nitrogen and oxygen molecules from ambient air, resulting in increased reactive oxygen and nitrogen species (RONS) production, which synergistically interacts with argon. This substantial generation of RONS establishes Ar–Air plasma jet as an effective method for treating 4-NP contamination in deionized water (DW). Notably, the Ar-Air plasma jet treatment outperforms that of the Ar jet. It achieves a higher degradation rate of 97.2% and a maximum energy efficiency of 57.3 gkW−1h−1, following a 6-min (min) treatment with 100 mgL−1 4-NP in DW. In contrast, Ar jet treatment yielded a lower degradation rate and an energy efficiency of 75.6% and 47.8 gkW−1h−1, respectively, under identical conditions. Furthermore, the first-order rate coefficient for 4-NP degradation was measured at 0.23 min−1 for the Ar plasma jet and significantly higher at 0.56 min−1 for the Ar–Air plasma jet. Reactive oxygen species, such as hydroxyl radical and ozone, along with energy from excited species and plasma-generated electron transfers, are responsible for CPJ-assisted 4-NP breakdown. In summary, this study examines RONS production from Ar and Ar–Air plasma jets, evaluates their 4-NP removal efficacy, and investigates the biocompatibility of 4-NP that has been degraded after plasma treatment.

Essential oil from Piper tuberculatum Jacq. (Piperaceae) and its majority compound β-caryophyllene: mechanism of larvicidal action against Aedes aegypti (Diptera: Culicidae) and selective toxicity.

Synthetic insecticides have been the primary approach in controlling Aedes aegypti; however, their indiscriminate use has led to the development of resistance and toxicity to non-target animals. In contrast, essential oils (EOs) are alternatives for vector control. This study investigated the mechanism of larvicidal action of the EO and β-caryophyllene from Piper tuberculatum against A. aegypti larvae, as well as evaluated the toxicity of both on non-target animals. The EO extracted from P. tuberculatum leaves was majority constituted of β-caryophyllene (54.8%). Both demonstrated larvicidal activity (LC50 of 48.61 and 57.20ppm, p < 0.05), acetylcholinesterase inhibition (IC50 of 57.78 and 71.97ppm), and an increase in the production of reactive oxygen and nitrogen species in larvae after exposure to the EO and β-caryophyllene. Furthermore, EO and β-caryophyllene demonstrate no toxicity to non-target animals Toxorhynchites haemorrhoidalis, Anisops bouvieri, and Diplonychus indicus (100% of survival rate), while the insecticide α-cypermethrin was highly toxic (100% of death). The results demonstrate that the EO from P. tuberculatum and β-caryophyllene are important larvicidal agents.

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection.

Despite the significant progress in the fields of biology, physiology, molecular medicine, and pharmacology; the designation of the properties of nitrogen monoxide in the regulation of life-supporting functions of the organism; and numerous works devoted to this molecule, there are still many open questions in this field. It is widely accepted that nitric oxide (•NO) is a unique molecule that, despite its extremely simple structure, has a wide range of functions in the body, including the cardiovascular system, the central nervous system (CNS), reproduction, the endocrine system, respiration, digestion, etc. Here, we systematize the properties of •NO, contributing in conditions of physiological norms, as well as in various pathological processes, to the mechanisms of cytoprotection and cytodestruction. Current experimental and clinical studies are contradictory in describing the role of •NO in the pathogenesis of many diseases of the cardiovascular system and CNS. We describe the mechanisms of cytoprotective action of •NO associated with the regulation of the expression of antiapoptotic and chaperone proteins and the regulation of mitochondrial function. The most prominent mechanisms of cytodestruction-the initiation of nitrosative and oxidative stresses, the production of reactive oxygen and nitrogen species, and participation in apoptosis and mitosis. The role of •NO in the formation of endothelial and mitochondrial dysfunction is also considered. Moreover, we focus on the various ways of pharmacological modulation in the nitroxidergic system that allow for a decrease in the cytodestructive mechanisms of •NO and increase cytoprotective ones.

Understanding the Effect of Saturated Gases on Catalytic Performance of Graphitic Carbon Nitride (g‐C3N4) for H2O2 Generation and Dye Degradation in the Presence of Ultrasound

In this article, the effect of saturated gases on H2O2 generation and dye degradation is examined using graphitic carbon nitride (g‐C3N4) as a piezoelectric catalyst. A detailed catalytic evaluation is carried out using a double‐bath sono‐reactor, where the performance of g‐C3N4 for H2O2 production and degradation of rhodamine B and indigo carmine dyes is evaluated for a range of catalyst dosage levels and saturated gases. Specific gases are selected to understand their role in the sonochemical production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and to elucidate the catalytic mechanism. The use of an Ar–O2 gas mixture leads to the highest yield for H2O2 production and dye degradation due to the positive effect of argon and oxygen in the generation of H2O2 and ROS, respectively. The presence of nitrogen in both air and in an Ar–air mixture increases H2O2 generation since RNS improves the conversion of •OH into H2O2. In contrast, air and Ar–air negatively influences the generation of ROS, which results in a low rate of dye degradation. In this work, new insights of the mechanisms of sonochemical and piezocatalytic processes in the use of graphitic carbon nitride in catalytic applications are provided.

Redox behaviour of Cu-Aβ(4-16) complexes related to Alzheimer's Disease

The development of Alzheimer's Disease (AD) has been linked to abnormal quantities of β-amyloid peptides in the brain. The majority of studies have focussed on Aβ(1-40/42) amyloids and their Cu(II)-Aβ(1-40/42) complexes which are responsible for production of reactive oxygen and nitrogen species (ROS and RNS), which are highly toxic to neurons. According to recent studies on amyloid plaques, Aβ(4–42), which is an N-truncated version of Aβ(1–42), is as prevalent as Aβ(1–42) in the brain. Although Cu(II) ions, bounded by Aβ(4–42), can be oxidized to highly reactive Cu(III) ions, its Cu(II) complexes do not appear to contribute to ROS/RNS formation. In this paper, the pH-dependent voltammetric response of Aβ(4–16)-Cu(II) complexes is investigated to understand the influence of the deprotonation of tyrosine within the complex towards the Cu(II)/Cu(III) reaction. The results will help to better understand the scavenging role of tyrosine in quenching highly reactive Cu(III) ions not only in Aβ(4-x)-Cu(II) complexes but also provide clues to the reactive properties of other tyrosine-containing amyloid-metal complexes.

Widespread S-persulfidation in activated macrophages as a protective mechanism against oxidative-inflammatory stress

Acute inflammatory responses often involve the production of reactive oxygen and nitrogen species by innate immune cells, particularly macrophages. How activated macrophages protect themselves in the face of oxidative-inflammatory stress remains a long-standing question. Recent evidence implicates reactive sulfur species (RSS) in inflammatory responses; however, how endogenous RSS affect macrophage function and response to oxidative and inflammatory insults remains poorly understood. In this study, we investigated the endogenous pathways of RSS biogenesis and clearance in macrophages, with a particular focus on exploring how hydrogen sulfide (H2S)-mediated S-persulfidation influences macrophage responses to oxidative-inflammatory stress. We show that classical activation of mouse or human macrophages using lipopolysaccharide and interferon-γ (LPS/IFN-γ) triggers substantial production of H2S/RSS, leading to widespread protein persulfidation. Biochemical and proteomic analyses revealed that this surge in cellular S-persulfidation engaged ∼2% of total thiols and modified over 800 functionally diverse proteins. S-persulfidation was found to be largely dependent on the cystine importer xCT and the H2S-generating enzyme cystathionine γ-lyase and was independent of changes in the global proteome. We further investigated the role of the sulfide-oxidizing enzyme sulfide quinone oxidoreductase (SQOR), and found that it acts as a negative regulator of S-persulfidation. Elevated S-persulfidation following LPS/IFN-γ stimulation or SQOR inhibition was associated with increased resistance to oxidative stress. Upregulation of persulfides also inhibited the activation of the macrophage NLRP3 inflammasome and provided protection against inflammatory cell death. Collectively, our findings shed light on the metabolism and effects of RSS in macrophages and highlight the crucial role of persulfides in enabling macrophages to withstand and alleviate oxidative-inflammatory stress.

Oxidative Stress and Cerebral Vascular Tone: The Role of Reactive Oxygen and Nitrogen Species.

The brain's unique characteristics make it exceptionally susceptible to oxidative stress, which arises from an imbalance between reactive oxygen species (ROS) production, reactive nitrogen species (RNS) production, and antioxidant defense mechanisms. This review explores the factors contributing to the brain's vascular tone's vulnerability in the presence of oxidative damage, which can be of clinical interest in critically ill patients or those presenting acute brain injuries. The brain's high metabolic rate and inefficient electron transport chain in mitochondria lead to significant ROS generation. Moreover, non-replicating neuronal cells and low repair capacity increase susceptibility to oxidative insult. ROS can influence cerebral vascular tone and permeability, potentially impacting cerebral autoregulation. Different ROS species, including superoxide and hydrogen peroxide, exhibit vasodilatory or vasoconstrictive effects on cerebral blood vessels. RNS, particularly NO and peroxynitrite, also exert vasoactive effects. This review further investigates the neuroprotective effects of antioxidants, including superoxide dismutase (SOD), vitamin C, vitamin E, and the glutathione redox system. Various studies suggest that these antioxidants could be used as adjunct therapies to protect the cerebral vascular tone under conditions of high oxidative stress. Nevertheless, more extensive research is required to comprehensively grasp the relationship between oxidative stress and cerebrovascular tone, and explore the potential benefits of antioxidants as adjunctive therapies in critical illnesses and acute brain injuries.

Dynamics of NO, N2O, and ONOOH in atmospheric-pressure air dielectric barrier discharge: decoupling energy density and gas temperature effects varying with discharge voltage

The dose regulation of reactive nitrogen species is crucial for biomedical applications. In this study, we develop a global chemical kinetics model comprising 92 species and 1018 reactions to investigate the regulatory dynamics of three types of reactive nitrogen species, i.e. NO, N2O, and ONOOH, which vary with the discharge voltage in an air coaxial dielectric barrier discharge. Based on the experimental results, the model can describe the density variations of NO, N2O, and ONOOH. The simulation results indicate that the O, NO3− , NO2− , and O3 are essential intermediate species related to NO generation; N, NO2, O-, N2*, and O(1D) are essential intermediate species related to N2O generation; and O2− , NO, NO2, OH, O4− , and O3 are essential intermediate species related to ONOOH generation. The individual and comprehensive effects of the energy density and gas temperature on the densities of NO, N2O, and ONOOH and the corresponding intermediate species are quantified under increasing discharge voltages. The simulation results indicate that the energy density is the primary factor affecting the number density of NO, N2O, and ONOOH, whereas the gas temperature exerts a completely different effect on these three species. These insights are valuable for plasma applications in biomedicine, where the selective and controlled production of reactive nitrogen species is key for achieving the desired plasma performance.

Dual Role of Alchemilla vulgaris L. Extract in Breast Cancer Regression: Reestablishment of Effective Immune Response.

Ethnomedicinal records have long mentioned the historical usage of Alchemilla vulgaris L. in folk medicine, particularly for the treatment of gynecological issues. Building on this ethnomedicinal knowledge regarding female illnesses, the aim of this research was to evaluate the impact of ethanolic extract of A. vulgaris on mouse breast cancer cells (4T1) in vitro and in vivo, in addition to its effect on the immune compartment in the tumor microenvironment. Behind viability decrease of 4T1 cells induced by treatment with A. vulgaris extract was strong inhibition of cell proliferation accompanied by caspase-dependent apoptosis and autophagic cell death. Observed changes in 4T1 cell culture after treatment were well orchestrated and led to a reduction in metastatic potential through weakened adhesion, invasion, migration, and colony-forming abilities in vitro. Enhanced intracellular production of reactive oxygen and nitrogen species promoted by the treatment might interfere with all the observed effects. Apart from the direct effect on tumor cells, the A. vulgaris extract significantly reduced tumor growth in the solid orthotropic mammary carcinoma model through restitution of efficient local and systemic immune response reflected in enhanced antigen-presenting potential of dendritic cells (DCs) as well as the extent and activity of effector T cells.

Comet Assay: Multifaceted Options for Studies of Plant Stress Response

Contrarily to chronic stresses, acute (i.e., fast and dramatic) changes in environmental factors like temperature, radiation, concentration of toxic substances, or pathogen attack often lead to DNA damage. Some of the stress factors are genotoxic, i.e., they damage the DNA via physical interactions or via interference with DNA replication/repair machinery. However, cytotoxic factors, i.e., those that do not directly damage the DNA, can lead to secondary genotoxic effects either via the induction of the production of reactive oxygen, carbon, or nitrogen species, or via the activation of programmed cell death and related endonucleases. The extent of this damage, as well as the ability of the cell to repair it, represent a significant part of plant stress responses. Information about DNA damage is important for physiological studies as it helps to understand the complex adaptive responses of plants and even to predict the outcome of the plant’s exposure to acute stress. Single cell gel electrophoresis (Comet assay) provides a convenient and relatively inexpensive tool to evaluate DNA strand breaks in the different organs of higher plants, as well as in unicellular algae. Comet assays are widely used in ecotoxicology and biomonitoring applications; however, they are still relatively rarely used in physiological studies. In this review, we provide an overview of the basic principles and of useful variations of the protocols of Comet assays, as well as of their use in plant studies, in order to encourage plant physiologists to include this tool in the analysis of plant stress responses.

Acute Antioxidant Response to Two Types of Exercises: 2000 M Run vs. Burpee Test.

Physical activity results in oxidative stress, as evidenced by the increased production of reactive oxygen, nitrogen species, and inflammatory mediators. The management of these components is instrumental for antioxidant adaptation to exercise and post-exercise recovery. Therefore, the present report aims to study the antioxidant response to two types of exercise (a 2000 m run and a burpee test) in healthy volunteers after a long period of inactivity (1-2 months). Antioxidant enzyme activities and oxidative stress markers (protein carbonyls and malondialdehyde content) were measured in neutrophils, peripheral blood mononuclear cells, and plasma. These parameters were determined under basal conditions and immediately post-exercise. Compared to those in basal state, neutrophil superoxide dismutase (28.3 vs. 22.9 pkat/109 cells), glutathione peroxidase (147.5 vs. 120.1 nkat/109 cells), and catalase (106.3 vs. 57.9 k/109 cells) were activated significantly (p < 0.05) after the burpee test. Peripheral blood mononuclear cells exhibited only significant (p < 0.05) catalase activation (113.6 vs. 89.4 k/109 cells) after the burpee test. Other enzymes, such as glutathione reductase and myeloperoxidase, tended to increase post-exercise, although the differences from baseline were not significant. Finally, compared to basal conditions, the protein carbonyl (24.5 vs. 14.5 mmol/L) and malondialdehyde (39.6 vs. 18.3 mmol/L) contents increased significantly (p < 0.05) in neutrophils and in plasma (115.1 vs. 97.8 and 130.2 vs. 123.4 μmol/L, respectively) after the burpee test. In conclusion, high-intensity exercise seems to induce immediate oxidative stress in inactive individuals, and the acute antioxidant response was slightly greater after the burpee test than after the 2000 m run. Glutathione-dependent antioxidant systems are activated immediately as protective mechanisms.

Nitric Oxide Plays a Dual Role in Cardiorenal Syndrome in Vitro Model.

Nitric oxide (NO) plays a dual role, acting as both an oxidant and a reducer, with various effects depending on its concentration and environment. Acute kidney injury's (AKI) pathogenesis observed in cardiorenal syndrome 3 (CRS 3) involves inflammatory responses and the production of reactive oxygen and nitrogen species. However, the role of NO on the development of CRS 3 is still not completely understood. The study aimed to mimic CRS 3 in vitro and investigate NO signaling and inflammatory molecules. Thus, HEK293 cells were submitted to normoxia (NX) or hypoxia (HX) protocols for 16 h followed by 3 h of reoxygenation, treated or not with L-NAME. Conditionate medium by HEK293 was transferred to H9c2 for 24 h. Cellular viability was evaluated by MTT assay, real time PCR was used to analyze gene expression and NO content were evaluated in the intra and extracellular medium by amperimetry. Carbonic anhydrase 9 (CA9) expression increased 2.9-fold after hypoxia. Hypoxia reduced 18 % cell viability in HEK293 that was restored by L-NAME treatment. The sum of nitrite (NO2-) and S-nitrosothiol (S-NO) fractions in HEK293 cells showed a substantial decrease on NO intracellular content (38 %). Both IL-6 and IL-10 decreased in all groups compared to NX cells. Besides TNF-α and Bax/Bcl2 ratio increased in hypoxia (approximately 120-fold and 600-fold, respectively) and L-NAME restored this effect. Regarding H9c2 cells, the S-NO fractions showed a substantial decrease in extracellular content after HX (17%) that was not restored by L-NAME. IL-1β decreases in cardiac cells treated with conditioned medium from HX/L-NAME. In conclusion this study highlights the complex interplay of NO and inflammatory factors in hypoxia-induced renal and cardiac cell responses, with potential implications for cardiorenal syndrome.

Disinfection Efficacy of Electrohydraulic Discharge Plasma against Xanthomonas campestris pv campestris: A Sustainable Seed Treatment Approach.

The prevalence of plant diseases caused by pathogens such as Xanthomonas campestris pv campestris (Xcc) poses a significant challenge to sustainable agriculture, necessitating the development of effective and eco-friendly disinfection methods. In this study, we investigated the efficacy of electrohydraulic discharge plasma (EHDP) as a promising alternative for disinfection against Xcc, a pathogen responsible for black rot in cruciferous vegetables. Unlike conventional gas-phase plasma, EHDP introduces two pivotal components: gas-liquid interface plasma (GLIP) and its consequential byproduct, plasma-activated water (PAW). While GLIP enables dual-phase production of reactive oxygen and nitrogen species (RONS), PAW is a reservoir of liquid-phase long-lived RONS, thereby enhancing its bactericidal efficacy. In our evaluations, we tested EHDP-induced GLIP and EHDP-induced PAW against Xcc cells in both in vitro (Xcc suspension) and in vivo (Xcc-inoculated cabbage seeds) settings, achieving noteworthy results. Within 15 min, these methods eliminated ∼98% of the Xcc cells in suspension. For in vivo assessments, nontreated seeds exhibited an infection rate of 98%. In contrast, both EHDP treatments showed a significant reduction, with ∼60% fewer seeds infected while maintaining ∼90% germination rate. In addition, the liquid-phase RONS in EHDP-PAW may enhance seed vigor with a faster germination rate within the initial 5 days. Remarkably, around 90% of EHDP-PAW-treated seeds yielded healthy seedlings, indicating dual benefits in bacterial suppression and seed growth stimulation. In contrast, the percentage of healthy seedlings from nontreated, Xcc-inoculated seeds was approximately 70%. Our research demonstrates the feasibility of using eco-friendly EHDP in the seed disinfection process.

Oxytocin alleviates periodontitis in adult rats.

The objective of the study was to evaluate the expression of oxytocin receptors in normal and inflamed gingiva, as well as the effects of systemic administration of oxytocin in bone loss and gum inflammatory mediators in a rat model of experimental periodontitis. Current evidence supports the hypothesis of a disbalance between the oral microbiota and the host's immune response in the pathogenesis of periodontitis. Increased complexity of the microbial biofilm present in the periodontal pocket leads to local production of nitrogen and oxygen-reactive species, cytokines, chemokines, and other proinflammatory mediators which contribute to periodontal tissue destruction and bone loss. Oxytocin has been suggested to participate in the modulation of immune and inflammatory processes. We have previously shown that oxytocin, nitric oxide, and endocannabinoid system interact providing a mechanism of regulation for systemic inflammation. Here, we aimed at investigating not only the presence and levels of expression of oxytocin receptors on healthy and inflamed gingiva, but also the effects of oxytocin treatment on alveolar bone loss, and systemic and gum expression of inflammatory mediators involved in periodontal tissue damage using ligature-induced periodontitis. Therefore, anti-inflammatory strategies oriented at modulating the host's immune response could be valuable adjuvants to the main treatment of periodontal disease. We used an animal model of ligature-induced periodontitis involving the placement of a linen thread (Barbour flax 100% linen suture, No. 50; size 2/0) ligature around the neck of first lower molars of adult male rats. The ligature was left in place during the entire experiment (7 days) until euthanasia. Animals with periodontitis received daily treatment with oxytocin (OXT, 1000 μg/kg, sc.) or vehicle and/or atosiban (3 mg/kg, sc.), an antagonist of oxytocin receptors. The distance between the cement-enamel junction and the alveolar bone crest was measured in stained hemimandibles in the long axis of both buccal and lingual surfaces of both inferior first molars using a caliper. TNF-α levels in plasma were determined using specific rat enzyme-linked immunosorbent assays (ELISA). OXT receptors, IL-6, IL-1β, and TNF-α expression were determined in gingival tissues by semiquantitative or real-time PCR. We show that oxytocin receptors are expressed in normal and inflamed gingival tissues in male rats. We also show that the systemic administration of oxytocin prevents the experimental periodontitis-induced increased gum expression of oxytocin receptors, TNF-α, IL-6, and IL-1β (p < .05). Furthermore, we observed a reduction in bone loss in rats treated with oxytocin in our model. Our results demonstrate that oxytocin is a novel and potent modulator of the gingival inflammatory process together with bone loss preventing effects in an experimental model of ligature-induced periodontitis.

The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.

Renal fibrosis is increasingly recognized as a global public health problem. Acute kidney injury (AKI) and chronic kidney disease (CKD) both result in renal fibrosis. Oxidative stress and inflammation play central roles in progressive renal fibrosis. Oxidative stress and inflammation are closely linked and form a vicious cycle in which oxidative stress induces inflammation through various molecular mechanisms. Ample evidence has indicated that a hyperactive nuclear factor kappa B (NF-ƙB) signaling pathway plays a pivotal role in renal fibrosis. Hyperactive NF-ƙB causes the activation and recruitment of immune cells. Inflammation, in turn, triggers oxidative stress through the production of reactive oxygen species and nitrogen species by activating leukocytes and resident cells. These events mediate organ injury through apoptosis, necrosis, and fibrosis. Therefore, developing a strategy to target the NF-ƙB signaling pathway is important for the effective treatment of renal fibrosis. This Review summarizes the effect of the NF-ƙB signaling pathway on renal fibrosis in the context of AKI and CKD (immunoglobulin A nephropathy, membranous nephropathy, diabetic nephropathy, hypertensive nephropathy, and kidney transplantation). Therapies targeting the NF-ƙB signaling pathway, including natural products, are also discussed. In addition, NF-ƙB-dependent non-coding RNAs are involved in renal inflammation and fibrosis and are crucial targets in the development of effective treatments for kidney disease. This Review provides a clear pathophysiological rationale and specific concept-driven therapeutic strategy for the treatment of renal fibrosis by targeting the NF-ƙB signaling pathway.