Search Results (218)

Reactive oxygen species (ROS) are among the most effective tools of the innate immune response against pathogenic microbes. The respiratory burst (RB) of polymorphonuclear leukocytes (PMNs) generates an electron current that reduces molecular oxygen to superoxide. Superoxide reacts to form hydrogen peroxide as a precursor to the highly bactericidal hypochlorous acid. Here, we investigated whether alterations in extracellular potassium concentration impact H₂O₂ production. Such changes may occur, for example, during massive cell death due to necrosis or due to trauma injuries when potassium diffuses out of the cells. We recorded H₂O₂ release over a 2 h period of RB under varying potassium concentrations. Except for 100 mM potassium chloride, which increased the time delay before detectable H₂O₂ production, none of the potassium concentrations had a substantial effect on RB. We further examined whether this effect depended on the specific monovalent ion species. When sodium or methanesulfonate was used instead of potassium or chloride, respectively, no changes in H₂O₂ production were observed. Cell volume measurements under different potassium concentrations showed that only 100 mM potassium chloride significantly shrank the cells. We propose that hypertonic stress is crucial for delaying RB in human granulocytes, whereas the RB itself is independent of the tested ionic species. Additionally, the conducted hypertonic stress experiments revealed an unexpected time-dependence during the course of the RB, showing that the first 6 min were almost inert to hyperosmotic stress. Full article

Plant respiratory burst oxidase homolog (Rboh) genes are integral to the production of reactive oxygen species (ROS) and the regulation of stress responses. Here, bioinformatic techniques were employed to identify eight PgRboh genes (PgRbohA–H) in the genome of pomegranate (Punica granatum L.) and conduct a systematic analysis of this family. The findings showed that all PgRbohs proteins possess characteristic NADPH oxidase domains and are predicted to be localized on the cell membrane. Experimental verification confirmed the membrane localization of PgRbohD and PgRbohE proteins. Phylogenetic analysis categorized the PgRbohs proteins into six distinct groups, suggesting potential functional divergence among these groups. Promoter analysis revealed a significant presence of cis-acting elements responsive to low-temperature and methyl jasmonate (MeJA). The expression of PgRboh genes was found to be tissue-specific. Additionally, real-time PCR (RT-qPCR) was used to analyze expression patterns in response to low-temperature stress that involves multiple PgRboh genes in the cold response process. Overall, our results lay an important foundation for subsequent studies on the cold resistance function of pomegranate Rboh genes and provides new ideas for the breeding of new cold-resistant pomegranate varieties. Full article

Our previous research has demonstrated the role of optimal temperatures and reactive oxygen species (ROS) in maintaining symptomless nonhost resistance (NHR) of barley to powdery mildews. However, the exact functions of temperature and ROS in NHR of plants, including barley, to viral infections are not known. Although barley is a nonhost for Tobacco mosaic virus (TMV), this virus can replicate in barley leaves at temperatures of ca. 30 °C. Here we elucidated the influence of short-term heat stress pre-treatments (30 °C, 3 h; heat shock at 49 °C, 20 s) on the symptomless NHR of barley to TMV and the role of the ROS superoxide (O₂^.−) in maintaining NHR. Heat stress and antioxidant (superoxide dismutase and catalase, SOD + CAT) treatments resulted in 50–100% higher TMV levels, while combined heat shock and SOD + CAT application caused further increases in TMV and appearance of cell and tissue death resembling a hypersensitive response (HR). An early (from 2 h after inoculation) burst of O₂^.− was essentially absent in TMV-infected barley exposed to short-term heat stress pre-treatments. Expression of barley genes regulating ROS (O₂^.−) metabolism (HvRBOHF2, HvSOD1) and cell death (HvBI-1) displayed an inverse correlation with TMV levels even at later time points (1–4 days after inoculation), implying a role in symptomless NHR, while increased levels of the antioxidant glutathione marked heat stress-induced suppression of NHR. We demonstrated that short-term heat stress and antioxidant treatments result in compromised NHR of barley to TMV, pointing to the role of optimal temperatures and ROS (O₂^.−) in symptomless NHR to virus infections. Full article

The pathogenic plant fungus Bipolaris maydis is responsible for southern corn leaf blight (SCLB), a widespread agricultural disease that significantly reduces maize yield in various agroecological zones. The present research focuses on characterizing the role of Trichoderma harzianum cellobiohydrolase (CBH) Thph2 in induced maize resistance to SCLB by triggering the production of reactive oxygen species (ROS) in leaves. First of all, we demonstrated the potential activities of Thph2 in triggering ROS burst and PDC in a model plant, Nicotiana benthamiana. Cell death, ROS burst, and programmed cell death (PCD) were observed in N. benthamiana leaves following transient expression of Thph2, indicating its defensive role against Sclerotinia sclerotiorum infection. The removal of the signal peptide from Thph2 resulted in the complete loss of the cell death phenotype and the accumulation of reactive oxygen species (ROS), confirming that Thph2 functions as a microbial elicitor that primes host plant immunity through ROS-mediated signaling, thereby inducing systemic resistance (ISR). Furthermore, the Thph2 protein conferred resistance against B. maydis in maize, significantly increasing reactive oxygen species (ROS) accumulation (1.5-fold compared to the control) at 48 h post-inoculation (hpi),and leading to the reduction in the lesion area of SCLB by 15.9% at 2 days post-inoculation (dpi). Our results demonstrated that the Thph2 protein markedly enhanced the expression of lox5, aos, and hpl in maize leaves, thereby confirming its function in triggering plant defense mechanisms primarily via the jasmonic acid signaling pathway. This research reveals new molecular mechanisms by which T. harzianum enhances plant defense and showcases the biocontrol efficacy of Thph2 against southern corn leaf blight (SCLB). Full article

Oxybenzone (OBZ), an organic ultraviolet filter, is an emerging contaminant posing severe threats to ecosystem health. Using tobacco (Nicotiana tabacum) as a model plant, this study investigated the alleviation mechanisms of exogenous silicon (Na₂SiO₃, Si) and bamboo-based biochar (Bc) under OBZ stress. We systematically analyzed physiological and biochemical responses, including phenotypic parameters, reactive oxygen species metabolism, photosynthetic function, chlorophyll synthesis, and endogenous hormone levels. Results reveal that OBZ significantly inhibited tobacco growth and triggered a reactive oxygen species (ROS) burst. Additionally, OBZ disrupted antioxidant enzyme activities and hormonal balance. Exogenous Bc mitigated OBZ toxicity by adsorbing OBZ, directly scavenging ROS, and restoring the ascorbate-glutathione (AsA-GSH) cycle, thereby enhancing photosynthetic efficiency, while Si alleviated stress via cell wall silicification, preferential regulation of root development and hormonal signaling, and repair of chlorophyll biosynthesis precursor metabolism and PSII function. The mechanisms of the two stress mitigators were complementary, Bc primarily relied on physical adsorption and ROS scavenging, whereas Si emphasized metabolic regulation and structural reinforcement. These findings provide practical strategies for simultaneously mitigating organic UV filter pollution and enhancing plant resilience in contaminated soils. Full article

In this investigation, a hierarchical FeCo-layered double hydroxide (FeCo-LDH) electrochemical membrane material was prepared by a simple in situ hydrothermal method. The prepared material formed a 3D honeycomb-structured FeCo-LDH-modified carbon felt (FeCo-LDH/CF) catalytic layer with uniform open pores on a CF substrate with excellent catalytic activity and was served as the cathode in a flow-through electro-Fenton (FTEF) reactor. The electrocatalyst demonstrated excellent treatment performance (99%) in phenol simulated wastewater (30 mg L⁻¹) under the optimized operating conditions (applied voltage = 3.5 V, pH = 6, influent flow rate = 15 mL min⁻¹) of the FTEF system. The high removal rate could be attributed to (i) the excellent electrocatalytic oxidation performance and low interfacial charge transfer resistance of the FeCo-LDH/CF electrode as the cathode, (ii) the ability of the synthesized FeCo-LDH to effectively promote the conversion of H₂O₂ to •OH under certain conditions, and (iii) the flow-through system improving the mass transfer efficiency. In addition, the degradation process of pollutants within the FTEF system was additionally illustrated by the •OH dominant ROS pathway based on free radical burst experiments and electron paramagnetic resonance tests. This study may provide new insights to explore reaction mechanisms in FTEF systems. Full article

Background: Verticillium wilt (VW), caused by the fungal pathogen Verticillium dahliae, is a destructive disease that severely compromises cotton yield and fiber quality. Pyrimidine nucleotides, as essential metabolites and nucleic acid components, play critical roles in plant development and stress responses. However, genes involved in pyrimidine metabolism, especially their roles in disease resistance, remain largely uncharacterized in plants. Methods: Ghir_D05G039120, a gene encoding uridine kinase, shown to be associated with VW resistance in our previous study, was cloned and named as GhUKL4. The differential expression of GhUKL4 between the resistant and susceptible cultivars at multiple time points post-inoculation with V. dahliae was analyzed by quantitative real-time PCR (qRT-PCR), and the uracil phosphoribosyl transferase (UPRT) and uridine 5′-monophosphate kinase (UMPK) domains were verified by analyzing the amino acid sequences of GhUKL4. The role of GhUKL4 in the defense against VW infection was estimated by silencing GhUKL4 in the resistant and susceptible cultivars using virus-induced gene silencing (VIGS) analysis. Results: There were significant differences in the expression level of Ghir_D05G039120/ GhUKL4 among resistant and susceptible cotton lines. GhUKL4 contains UPRTase and UMPK domains, and there was one SNP between the resistant and susceptible cultivars in its 3′-UTR region. The silencing of GhUKL4 reduced cotton’s resistance to VW through mediating hormone signaling (JA) and oxidative stress (ROS) pathways. Conclusions: GhUKL4, encoding UMPK and UPRTase domain proteins, is a new regulatory factor associated with VW resistance in Gossypium hirsutum through fine-tuning JA-signalling and ROS bursting. Full article

We have previously shown that the mitochondrial respiratory chain (RC) can switch between the following two states: (i) an “ATP-producing” state characterized by the low production of reactive oxygen species (ROS), the vigorous translocation of hydrogen ions (H⁺), and the storage of energy from the H⁺ gradient in the form of ATP, and (ii) an “ROS-producing” state, where the translocation of H⁺ is slow but the production of ROS is high. Here, we suggest that the RC transition from an ATP-producing to an ROS-producing state initiates a mitochondrial permeability transition (MPT) by generating a burst of ROS. Numerous MPT activators induce the transition of the RC to an ROS-producing state, and the ROS generated in this state activate the MPT. The MPT, in turn, induces changes in conditions that are necessary for the RC to return to an ATP-producing state, decreasing the ROS production rate and restoring the normal permeability of the inner membrane. In this way, the transient MPT prevents cell damage from oxidative stress that would occur if the RC remained in an ROS-producing state. It is shown that an overload of glutamate, which enters through excitatory amino acid transporters (EAATs), induces the RC to switch to an ROS-producing state. Subsequent MPT activation causes a transition back to an ATP-producing state. The model was used to predict the spatial–temporal dynamics of glutamate concentrations and H₂O₂ production rates in a three-dimensional digital phantom of nervous tissue. Full article

The growing prevalence of bacterial infections and the alarming rise of antimicrobial resistance (AMR) have driven the need for innovative antimicrobial coatings for medical implants and biomaterials. However, implant surface properties, such as roughness, chemistry, and reactivity, critically influence biological interactions and must be engineered to ensure biocompatibility, corrosion resistance, and sustained antibacterial activity. This review evaluates three principal categories of antimicrobial agents utilized in surface functionalization: metal/metaloxide nanoparticles, antibiotics, and phytochemical compounds. Metal/metaloxide-based coatings, especially those incorporating silver (Ag), zinc oxide (ZnO), and copper oxide (CuO), offer broad-spectrum antimicrobial efficacy through mechanisms such as reactive oxygen species (ROS) generation and bacterial membrane disruption, with a reduced risk of resistance development. Antibiotic-based coatings enable localized drug delivery but often face limitations related to burst release, cytotoxicity, and diminishing effectiveness against multidrug-resistant (MDR) strains. In contrast, phytochemical-derived coatings—using bioactive plant compounds such as curcumin, eugenol, and quercetin—present a promising, biocompatible, and sustainable alternative. These agents not only exhibit antimicrobial properties but also provide anti-inflammatory, antioxidant, and osteogenic benefits, making them multifunctional tools for implant surface modification. The integration of these antimicrobial strategies aims to reduce bacterial adhesion, inhibit biofilm formation, and enhance tissue regeneration. By leveraging the synergistic effects of metal/metaloxide nanoparticles, antibiotics, and phytochemicals, next-generation implant coatings hold the potential to significantly improve infection control and clinical outcomes in implant-based therapies. Full article

Citral, an organic compound found in lemongrass (Cymbopogon citratus) oil and Litsea cubeba essential oil, has been reported to exhibit notable antifungal activity against Magnaporthe oryzae (M. oryzae), the pathogen of rice blast, which causes significant economic losses in rice production. However, the role of citral in inducing oxidative stress related to antifungal ability and its underlying regulatory networks in M. oryzae remain unclear. In this study, we investigated the oxidative effects of citral on M. oryzae and conducted transcriptomic and widely targeted metabolomic (WTM) analyses on the mycelia. The results showed that citral induced superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) activities but reduced glutathione S-transferase (GST) activity with 25% maximal effective concentration (EC₂₅) and 75% maximal effective concentration (EC₇₅). Importantly, citral at EC₇₅ reduced the activities of mitochondrial respiratory chain complex I, complex III and ATP content, while increasing the activity of mitochondrial respiratory chain complex II. In addition, citral triggered a burst of reactive oxygen species (ROS) and a loss of mitochondrial membrane potential (MMP) through the observation of fluorescence. Furthermore, RNA-seq analysis and metabolomics analysis identified a total of 466 differentially expression genes (DEGs) and 32 differential metabolites (DAMs) after the mycelia were treated with citral. The following multi-omics analysis revealed that the metabolic pathways centered on AsA, GSH and melatonin were obviously suppressed by citral, indicating a disrupted redox equilibrium in the cell. These findings provide further evidences supporting the antifungal activity of citral and offer new insights into the response of M. oryzae under oxidative stress induced by citral. Full article

Chaperonin 60 proteins plays an important role in plant growth and development as well as the response to abiotic stress. As part of the protein homeostasis system, molecular chaperones have attracted increasing attention in recent years due to their involvement in the folding and assembly of key proteins in photosynthesis. However, little is known about the function of maize chaperonin 60 protein. In the study, a gene encoding the chaperonin 60 proteins was cloned from the maize inbred line B73, and named ZmCpn60-3. The gene was 1, 818 bp in length and encoded a protein consisting of 605 amino acids. Phylogenetic analysis showed that ZmCpn60-3 had high similarity with OsCPN60-1, belonging to the β subunits of the chloroplast chaperonin 60 protein family, and it was predicted to be localized in chloroplasts. The ZmCpn60-3 was highly expressed in the stems and tassels of maize, and could be induced by exogenous plant hormones, mycotoxins, and pathogens; Overexpression of ZmCpn60-3 in Arabidopsis improved the resistance to Pst DC3000 by inducing the hypersensitive response and the expression of SA signaling-related genes, and the H₂O₂ and the SA contents of ZmCpn60-3-overexpressing Arabidopsis infected with Pst DC3000 accumulated significantly when compared to the wild-type controls. Experimental data demonstrate that flg22 treatment significantly upregulated transcriptional levels of the PR1 defense gene in ZmCpn60-3-transfected maize protoplasts. Notably, the enhanced resistance phenotype against Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) in ZmCpn60-3-overexpressing transgenic lines was specifically abolished by pretreatment with ABT, a salicylic acid (SA) biosynthetic inhibitor. Our integrated findings reveal that this chaperonin protein orchestrates plant immune responses through a dual mechanism: triggering a reactive oxygen species (ROS) burst while simultaneously activating SA-mediated signaling cascades, thereby synergistically enhancing host disease resistance. Additionally, yeast two-hybrid assay preliminary data indicated that ZmCpn60-3 might bind to ZmbHLH118 and ZmBURP7, indicating ZmCpn60-3 might be involved in plant abiotic responses. The results provided a reference for comprehensively understanding the resistance mechanism of ZmCpn60-3 in plant responses to abiotic or biotic stress. Full article

Reactive oxygen species (ROS) are critical signalling molecules, but their overproduction leads to oxidative stress (OS), a common denominator in the pathogenesis of numerous non-communicable diseases (NCDs) and aging. General antioxidant therapies have largely been unsuccessful, highlighting the need for a deeper understanding of ROS amplification mechanisms to develop targeted interventions. This review proposes a unified, self-amplifying “vicious cycle” of inter-organelle crosstalk that drives pathological ROS elevation and cellular damage. We outline a pathway initiated by extracellular stressors that co-activate plasma membrane TRPM2 channels and NADPH oxidase-2. This synergy elevates cytoplasmic Ca²⁺, leading to lysosomal dysfunction and permeabilization, which in turn releases sequestered Zn²⁺. Mitochondrial uptake of this labile Zn²⁺ impairs electron transport chain function, particularly at Complex III, resulting in mitochondrial fragmentation, loss of membrane potential and a burst of mitochondrial ROS (mtROS). These mtROS diffuse to the nucleus, activating PARP-1 and generating ADPR, which further stimulates TRPM2, thereby perpetuating the cycle. This “circular domino effect” integrates signals generated across the plasma membrane (Ca²⁺), lysosomes (Zn²⁺), mitochondria (ROS) and nucleus (ADPR), leading to progressive organelle failure, cellular dysfunction, and ultimately cell death. Understanding and targeting specific nodes within this TRPM2-NOX2-Ca²⁺-Zn²⁺-mtROS-ADPR axis offers novel therapeutic avenues for NCDs by selectively disrupting pathological ROS amplification while preserving essential physiological redox signalling. Full article

Daytime-restricted feeding (TRF) exerts outstanding effects on circadian physiology, nutrient utilization, and energy metabolism. Limiting feeding access to two hours during the daytime (12:00–14:00 h) for three weeks promotes food-anticipatory activity (FAA). FAA encompasses not only behaviors related to meal expectations but also includes diurnal fluctuations in liver metabolic responses, including distinct redox handling. Hepatic microarray profiles of genes associated with redox response processes were analyzed at three crucial time points: at the beginning of the light period or before FAA (08:00 h), during the expression of FAA (11:00 h), and after feeding (14:00 h). Data on fasting and nutrient processing were integrated, whereas circadian implications were extrapolated by comparing the TRF transcriptional output with a one-day fasting group. Transcripts of redox reactions, such as reactive oxygen species (ROS) generation, antioxidant defenses, NAD⁺/NADH equilibrium, and glutathione, hydrogen peroxide (H₂O₂), arginine, nitric oxide (NO), and hydrogen sulfide (H₂S) metabolism, were analyzed. Results showed a decline in antioxidant defenses at 08:00 h, followed by a burst of pro-oxidant reactions, preparation of glutathione metabolism factors, and a tendency to decrease H₂O₂ and increase NO and H₂S during the FAA. Most of the findings observed during the FAA were absent in response to one-day fasting. Hence, TRF involves concerted and sequential responses in liver pro-oxidant and antioxidant reactions, facilitating a redox-related circadian control that optimizes the metabolic utilization of nutrients, which differs from a response to a simple fast-feed cycle. Full article

The phytotoxicity of aluminum (Al) to plants is well known. Auxin accumulation and reactive oxygen species (ROS) burst induced by Al toxicity are the key factors in root growth inhibition. Yucasin, an auxin synthesis inhibitor, effectively ameliorates Al phytotoxicity in tomato seedlings. However, the physiological mechanisms by which yucasin alleviates Al phytotoxicity in tomatoes remain elusive. Here, we examined the regulatory mechanisms of yucasin involved in tomato seedling growth under Al conditions through phenotypic, plant physiology analysis, and cellular experiments. Exogenous indole-3-acetic acid (IAA) application increased Al accumulation in tomato seedling roots, while yucasin decreased Al accumulation. Yucasin application reduced Al-induced ROS accumulation, lipid peroxidation, and cell death, enhanced root viability, and promoted tomato seedling root growth. Further, yucasin enhanced the antioxidant enzyme activities of superoxide dismutase, catalase, and peroxidase in plants under Al conditions. The results suggest that yucasin improves the scavenging capacity of ROS by maintaining the activities of antioxidative enzymes. This study elucidates the physiological mechanism by which yucasin alleviates Al phytotoxicity, highlighting its potential to enhance plant tolerance under acidic Al conditions. Full article

Reactive oxygen species (ROS) are toxic by-products of aerobic cellular metabolism. However, ROS conduct multiple functions, and specific ROS sources can have beneficial or detrimental effects on plant health. This review explores the complex dynamics of ROS in plant defense mechanisms, focusing on their involvement in basal resistance, hypersensitive response (HR), and systemic acquired resistance (SAR). ROS, including superoxide anion (O²⁻), singlet oxygen (¹O₂), hydroxyl radicals (OH), and hydrogen peroxide (H₂O₂), are generated through various enzymatic pathways. They may serve to inhibit pathogen growth while also activating defense-related gene expression as signaling molecules. Oxidative damage in cells is mainly attributed to excess ROS production. ROS produce metabolic intermediates that are involved in various signaling pathways. The oxidative burst triggered by pathogen recognition initiates hyper-resistance (HR), a localized programmed cell death restricting pathogen spread. Additionally, ROS facilitate the establishment of SAR by inducing systemic signaling networks that enhance resistance across the plant. The interplay between ROS and phytohormones such as jasmonic acid (JA), salicylic acid (SA), and ethylene (ET) further complicates this regulatory framework, underscoring the importance of ROS in orchestrating both local and systemic defense responses. Grasping these mechanisms is essential for creating strategies that enhance plant resilience to biotic stresses. Full article