Search Results (1,743)

Soil salinity disrupts redox homeostasis and limits plant growth and development. Although catalase (CAT) and superoxide dismutase (SOD) are key enzymatic antioxidants, the CAT and SOD gene families have not been characterized in Artemisia argyi (A. argyi), a species of medicinal and ecological importance. While SOD and CAT serve as the primary enzymatic scavengers for reactive oxygen species (ROS) detoxification, their genomic architecture and stress-responsive regulatory networks in A. argyi have remained uncharacterized. In this study, we conducted the first comprehensive genome-wide analysis of these gene families in A. argyi, identifying 22 structurally conserved members (8 AarCATs and 14 AarSODs). Collinearity and synteny analyses revealed strict lineage-specific evolutionary conservation, while tertiary protein modeling and subcellular localization illustrated a highly organized multi-organelle defense compartmentalization. High salinity (up to 200 mM NaCl) reduced the stomatal conductance and net photosynthetic rate. Salt stress reduced growth and increased osmoprotectant and antioxidant accumulation in A. argyi. Furthermore, histochemical staining using nitroblue tetrazolium (NBT) and 3,3′-Diaminobenzidine (DAB) provided comprehensive evidence of significant accumulation of ROS in leaves, which indicates the intense oxidative stress triggered by ionic stress. Tissue-specific analysis revealed that AarCAT1, AarCSD1, and AarFSD2 were 3.9-, 7.9-, and 12.7-fold higher in leaves than in roots, respectively. Under stress, AarCAT6 and AarCSD1 were strongly repressed in leaves by ~50% and ~46–70%, respectively, whereas AarMSD2 and AarMSD3 were significantly induced in roots by ~2.2- and ~1.8-fold. These distinct expression patterns suggest their potential involvement in tissue-specific stress adaptation and ROS homeostasis. These findings uncover the evolutionary and physiological basis of salt tolerance in A. argyi, providing genetic targets for climate-resilient breeding. Full article

Background/Objectives: The oxidation of low-density lipoprotein (LDL) is a crucial step in atherogenesis. Beta-Caryophyllene (BCP) is a natural compound with established anti-oxidative and anti-inflammatory properties as shown in animal and cell culture studies. We examined whether BCP can impede LDL oxidation in an in vitro model. Methods: The anti-oxidative effect of BCP was evaluated in different concentrations (0, 25, 50, 100, and 150 µg/mL) with regard to scavenging reactive oxygen species (ROS) during LDL oxidation, which was initiated by the addition of copper chloride (CuCl₂) in a concentration of 10 µmol/L. Lipid hydroperoxides (LPO), malondialdehyde (MDA), dienes, cell viability, and reactions of BCP with ROS according to Gibbs free energies were applied to determine the oxidation state of LDL. Results: Our findings indicated that BCP is highly efficient in inhibiting LDL oxidation in a dose-dependent manner in this in vitro model. The lipid hydroperoxide content in oxLDL was significantly lower in the presence of 100 µg/mL BCP compared to oxLDL without BCP (p < 0.0001). This corresponds to the MDA levels, which were significantly lower in the presence of 100 µg/mL BCP compared to oxLDL without BCP (p = 0.0393). Furthermore, a dose-dependent inhibition of diene formation in the LDL particle was observed in the presence of ascending BCP concentrations which corresponds to a decrease in the cytotoxicity of oxLDL in EA.hy926 cells in the presence of increasing concentrations of BCP. Moreover, BCP’s anti-oxidant effectiveness exceeds that of the widely recognized anti-oxidant spermidine at equivalent concentrations. Our quantum chemical calculations showed that the reactions between BCP and hydroxyl radicals, hydroperoxyl radicals, or hydrogen peroxide are exergonic. We therefore conclude that BCP impedes the oxidation of LDL by its capability to scavenge (at least) these three reactive oxygen species. Conclusions: Our results indicate that BCP impedes the oxidation of LDL in vitro and therefore presumably has the potential to serve as an appropriate therapeutic agent to prevent atherogenesis and related (cardio)vascular diseases by balancing vascular oxidative stress. For this purpose, more prospective clinical studies in humans are required to assess the potential atheroprotective and health-promoting effects of BCP. Full article

Hydrogel bio-adhesives have gained great attention in wound healing and tissue regeneration applications because conventional wound closures are often hindered by insufficient adhesion and poor biocompatibility. Considering that dynamic covalent interactions facilitate robust wet adhesion in hydrogels, we fabricated a Schiff base hydrogel bio-adhesive based on oxidized chondroitin sulfate (OCS) and polyethylenimine (PEI), and employed different degrees of OCS oxidation to regulate the physicochemical properties of the bio-adhesives. In this system, aldehyde groups of OCS react with amino groups of PEI to form covalent imine crosslinks, while physical hydrogen bonds also contribute as supplementary interactions. The fabricated hydrogel bio-adhesives demonstrated a three-dimensional interconnected microstructure and regulated equilibrium swelling ratios. The rheological tests also confirmed the typical viscoelasticity of the hydrogels and their shear-thinning behavior. The obtained hydrogel bio-adhesives demonstrated rapid and autonomous self-healing ability and strong adhesion to the surfaces of various matrices and wet organs, including wood, glass, metal, plastic, rubber, and heart, liver, spleen, stomach, and lung tissue. Furthermore, an ABTS radical scavenging assay confirmed their potent antioxidant activity. The hydrogels possessed effective antibacterial activities against Gram-positive Staphylococcus aureus and Gram-negative Escherichia coli. The hydrogels exhibited good hemocompatibility, effective intracellular reactive oxygen species (ROS) scavenging activity, favorable cytocompatibility, and promoted cell proliferation. These results confirmed the fabricated hydrogels via Schiff base connections for biomedical applications and provided a facile design for biomedical hydrogel bio-adhesives. Full article

Drought is one of the major environmental constraints limiting tomato growth and productivity. Identifying regulators that enhance drought tolerance without compromising plant growth is therefore important for tomato production. Homeodomain-leucine zipper (HD-Zip) transcription factors (TFs) play essential roles in plant development and abiotic stress responses; however, the functions of most HD-Zip II members in tomato remain poorly understood. Here, we identified SlHZ07, a drought-responsive HD-Zip II TF, through transcriptome analysis and characterized its biological function in tomato. SlHZ07 was rapidly induced by drought stress and localized predominantly to the nucleus. Overexpression of SlHZ07 significantly enhanced drought tolerance, whereas RNAi-mediated suppression increased drought sensitivity. Physiological analyses showed that SlHZ07 overexpression reduced reactive oxygen species (ROS) accumulation, enhanced antioxidant enzyme activities, upregulated expression of ROS-scavenging genes, and alleviated membrane damage under drought stress. Hormone analyses revealed that SlHZ07 positively regulated jasmonic acid (JA) accumulation and the expression of JA biosynthetic genes, including OPR2, OPR3, JAR1, and AOC, but did not alter endogenous abscisic acid (ABA) levels under well-watered conditions. Furthermore, SlHZ07 promoted vegetative growth by increasing endogenous gibberellin (GA) levels and upregulating the expression of the GA biosynthetic genes GA20ox2 and GA20ox4. Together, our findings identify SlHZ07 as a previously uncharacterized positive regulator that coordinates plant growth and drought adaptation by integrating GA biosynthesis, JA homeostasis, and ROS detoxification. These results expand our understanding of HD-Zip II TFs and provide a promising genetic target for improving drought tolerance in tomato. Full article

Stanniocalcin-1 (STC-1) is a multifunctional glycoprotein; however, its role in protecting intestinal epithelial cells against oxidative injury has not been completely elucidated. This study investigated the cytoprotective effects and underlying molecular mechanisms of STC-1 overexpression in porcine intestinal epithelial (IPEC-J2) cells subjected to tert-butyl hydroperoxide (TBHP)-induced oxidative stress. IPEC-J2 cells were transfected with pcDNA3.1/STC-1 prior to TBHP challenge. STC-1 overexpression markedly rescued cells from TBHP-induced cytotoxicity and cell death, and was associated with a reduced Bax/Bcl-2 ratio. Concurrently, elevated STC-1 expression dramatically suppressed intracellular reactive oxygen species and mitochondrial superoxide accumulation while preserving the mitochondrial membrane potential. These physiological improvements were accompanied by enhanced total antioxidant capacity and activities of key antioxidant enzymes. Mechanistically, STC-1 overexpression enhanced autophagic flux and promoted Pink1/Parkin-mediated mitophagy to eliminate dysfunctional mitochondria. Furthermore, STC-1 upregulation potentiated the AMPK–Nrf2/Sirt1 signaling axis and the subsequent transcriptional upregulation of mitochondrial quality control markers, including FoxO1, PGC-1α, and TFAM, under stress conditions. Collectively, these findings demonstrate that STC-1 safeguards porcine intestinal cells against oxidative injury by orchestrating a cooperative defense network encompassing ROS scavenging, mitochondrial homeostasis, and antioxidant defense amplification via the AMPK–Nrf2/Sirt1 pathway, highlighting a potential therapeutic target for preventing stress-associated intestinal disorders in piglets. Full article

Radiation-induced salivary gland injury (RISGI) is an inevitable and serious complication for patients with head and neck cancer. Reactive oxygen species (ROS) generated during radiotherapy are the primary cause. Hyposalivation is the most obvious symptom of RISGI. Currently, clinical interventions have not achieved the desired efficacy. Inspired by the radioprotective properties of Mn₃O₄ and PDA nanozymes and the robust bioadhesive properties of PDA hydrogels, we designed a Mn₃O₄–polydopamine hybrid hydrogel (termed MP hydrogel) capable of alleviating radiation-induced hyposalivation. MP hydrogel effectively scavenges ROS and increases the viability of salivary gland cells under ionizing radiation (IR). As a proof of concept, we applied MP hydrogel to the submandibular glands (SMGs) of male Sprague–Dawley (SD) rats, one of the three major salivary glands of rats. We demonstrated that MP hydrogel effectively mitigated radiation-triggered hyposalivation after in situ gelation in rats. Full article

Oil palm (Elaeis guineensis Jacq.) is a quintessential tropical oilseed crop, whose distribution and yield are significantly constrained by low-temperature stress. This study conducted physiological and proteomic analyses to investigate the early response mechanisms of one-year-old thin-shelled oil palm seedlings exposed to low temperatures of 8 °C for durations of 0, 0.5, 1, 2, 4, and 8 h. The results indicated that low-temperature treatment inhibited chlorophyll accumulation, reduced photosynthetic efficiency, and increased the levels of malondialdehyde (MDA) and soluble sugars. Concurrently, the activities of antioxidant enzymes exhibited a transient increase, suggesting an imbalance in the antioxidant defense system during the later stages of stress. Proteomics results indicate that the core pathways involved are fatty acid degradation and the regulatory pathways for starch and sucrose metabolism. Within these pathways, key proteins such as ACSL (long-chain fatty acid-CoA ligase), paaF (enoyl-CoA hydratase), HADH (3-hydroxyacyl-CoA dehydrogenase), and HADHA (enoyl-CoA hydratase/long-chain 3-hydroxyacyl-CoA dehydrogenase) are identified among 13 differential accumulation protein (DAPs). It is hypothesized that these key proteins work in concert to regulate osmosis, scavenge reactive oxygen species (ROS), stabilize membranes, and supply energy. Through physiological and proteomic analyses, this study identified physiological indicators, key proteins, and regulatory pathways associated with cold tolerance in oil palm, thus providing a theoretical basis for breeding low-temperature-tolerant oil palm varieties. The findings contribute to the development of low-temperature-tolerant oil palm cultivars. Full article

Pressure ulcers are a major clinical problem in patients with severe immobility; however, their pathophysiology extends beyond mechanical pressure and localized ischemia. Repetitive ischemia–reperfusion promotes sustained reactive oxygen species (ROS) production, leading to persistent inflammation, mitochondrial dysfunction, metabolic stress, and chronic wound refractoriness. In this review, we propose the ROS Gatekeeper Hypothesis, in which a ROS-dominant redox microenvironment functions as the central determinant of signaling permissiveness for gaseous signaling molecules. Within this framework, nitric oxide (NO) serves as the principal redox-responsive signaling axis, whereas hydrogen sulfide (H2S) and carbon monoxide (CO) function as complementary redox-responsive modulators whose biological effects depend on the surrounding redox environment. Under ROS-dominant conditions, NO bioavailability is reduced through superoxide scavenging and endothelial nitric oxide synthase (eNOS) uncoupling, while progressive oxidative stress is proposed to drive a transition toward a redox-constrained state in which responsiveness to all three gasotransmitters becomes increasingly limited. Accordingly, therapeutic efficacy is proposed to depend on preservation or restoration of signaling permissiveness rather than gasotransmitter abundance alone. The ROS Gatekeeper Hypothesis provides a unified conceptual framework for interpreting heterogeneous therapeutic responses and guiding future stage-specific, redox-oriented therapeutic strategies for chronic wounds. Full article

Superoxide dismutase 2 (SOD2), a key mitochondrial antioxidant enzyme, is essential for maintaining cellular redox homeostasis by scavenging superoxide radicals. While viruses often induce oxidative stress, the specific role of SOD2 in antiviral defense remains unclear. Here, we report that vaccinia virus (VACV) infection triggers mitochondrial and cellular reactive oxygen species (ROS) and selectively upregulates SOD2, but not SOD1. Genetic knockout of SOD2 exacerbated mitochondrial ROS (mtROS) accumulation and significantly enhanced VACV replication and spread, resulting in larger viral plaques. Conversely, SOD2 overexpression constrained plaque formation and suppressed viral dissemination. Mechanistically, the antiviral function of SOD2 does not strictly rely on its enzymatic activity or mitochondrial targeting, as neither the deacetylation-mimicking mutant nor the mutant lacking the mitochondrial localization signal peptide appreciably impaired its antiviral potency. Furthermore, in a rabbit model, local overexpression of human SOD2 attenuated the poxvirus lesion formation. Our findings unveil an important yet easily overlooked role of SOD2 in antiviral defense and posit it as a promising candidate for the development of host-directed therapeutics against poxviruses. Full article

Puccinellia tenuiflora is a perennial halophytic grass commonly regarded as a pioneer species for the ecological restoration of saline–alkali land. Its adaptive capacity and subsequent utilization value are shaped by interacting structural, physiological, molecular, ecological, and management-related factors. This review summarizes recent studies on saline–alkali tolerance in P. tenuiflora, with emphasis on root structural barriers, Na⁺/K⁺ homeostasis, osmotic adjustment, organic-acid metabolism, antioxidant defense, ion transport, and multi-omics regulation. To better understand the integrated stress response, we propose a functional framework that distinguishes first-line defenses from downstream cellular repair mechanisms. First-line defenses include root apoplastic barriers (Casparian strips and suberization) that restrict Na⁺ entry, plasma-membrane Na⁺/H⁺ antiporters (e.g., SOS1) that mediate active Na⁺ exclusion, and K⁺-retention mechanisms (e.g., AKT1, HKT2;1) that preserve cytosolic K⁺/Na⁺ homeostasis—these operate rapidly to prevent ion imbalance at the onset of stress. Downstream repair and acclimation mechanisms include osmotic adjustment via compatible solutes (e.g., proline, glycine betaine), organic-acid accumulation (especially citric acid) for pH regulation and chelation, ROS scavenging systems, and proteomic/phosphoproteomic reprogramming that repair stress-induced damage and restore metabolic balance. Furthermore, saline–alkali stress involves both short-term osmotic shock and long-term ionic toxicity, and available evidence suggests a temporal shift in the relative importance of these mechanisms: osmotic adjustment and rapid ion exclusion dominate during the initial hours to days of stress, whereas organic-acid metabolism, ROS buffering, and molecular reprogramming become increasingly important during prolonged exposure, sustaining tissue integrity and enabling long-term persistence. Current evidence indicates that saline–alkali tolerance in P. tenuiflora results from the combined action of several processes, including restricted Na⁺ entry, K⁺ retention, organic-acid accumulation, reactive oxygen species homeostasis, and organ-specific molecular responses. This review also discusses the significance of P. tenuiflora in community establishment, saline–alkali land restoration, and post-restoration forage utilization. Field studies and limited feeding trials suggest that P. tenuiflora can provide biomass and utilization potential after community stabilization. However, based on current evidence, it is more appropriate to define its forage value as a post-restoration utilization extension rather than as that of a fully developed specialized forage crop. Further studies are required on nutritional quality, mineral-element safety, long-term field management, and animal feeding validation. Full article

Background/Objectives: Tissue bio-adhesives have gained significant attention as efficient alternatives to conventional wound closures, which are often hindered by insufficient adhesion and poor biocompatibility. Methods: Inspired by nature’s robust wet-adhesion strategies that use dynamic covalent interactions, we have reported a facilely fabricated hydrogel bio-adhesive based on lactobionic acid-conjugated polyethylenimine (LA-PEI) and oxidized dextran (ODex) via Schiff base linkages. Results: The prepared hydrogels exhibited three-dimensional interconnected porous networks, regulated swelling ratios, typical viscoelasticity, shear-thinning behavior, and self-healing ability. Notably, the swelling ratios of the hydrogels depended on composition, and OLP11 displayed the highest swelling ratio of over 1500%. The hydrogel bio-adhesives exhibited strong adhesion to various surfaces, including glass, metal, plastic, rubber, and wood, as well as to different chicken organs, including the heart, liver, spleen, and stomach. Furthermore, the hydrogels exhibited excellent ABTS radical-scavenging activity, effective intracellular reactive oxygen species (ROS) scavenging, and good hemocompatibility, with hemolysis ratios of all hydrogels close to 0%, below the threshold of 5%. After culturing with NIH 3T3 fibroblasts, the hydrogels demonstrated good cytocompatibility and promoted cell proliferation, with cell viabilities on day 3 reaching over 90%. Conclusions: This design yields multifunctional hydrogel bio-adhesives, showing strong promise for wound care and tissue repair applications. Full article

High-temperature stress severely limits the cultivation and ornamental quality of herbaceous peony, especially in low-latitude regions. The objective of this study was to reveal the potential mechanism involved in regulation of jasmonates on herbaceous peony heat tolerance through crosstalk between phytohormones and the reactive oxygen species (ROS) scavenging system. The study found that exogenous methyl jasmonate (MeJA) significantly improved thermotolerance of the low-latitude cultivar ‘Hang Baishao’ by enhancing antioxidase activities and modulating endogenous phytohormone levels. The MeJA-treated group exhibited markedly higher ratios of MeJA to zeatin riboside (ZR), gibberellic acid (GA₃), brassinolide (BR), and indole-3-acetic acid (IAA) compared with the control group; catalase (CAT) and superoxide dismutase (SOD) activities were significantly elevated relative to hydrogen peroxide (H₂O₂) content, with both ratios peaking at 36 h post-heat treatment. Transcriptomic results revealed that MeJA reshaped the expression of genes involved in jasmonic acid (JA) signaling and ROS scavenging, such as FAD4, MED25, and JAZ2 and CSD2/3, FSD1, and CAT3. Four modules including the hub genes CIPK5/6, WRKY19/40 and CYPs were identified from the weighted gene co-expression network analysis (WGCNA), which may be key players in coordinating JA signaling and antioxidant defense. This study demonstrates that MeJA enhanced herbaceous peony thermotolerance by orchestrating a regulatory network involving phytohormonal crosstalk and activation of the ROS scavenging system, and offers candidate genes for future exploration of function and interactions. Full article

Despite the traditional application of Sophora moorcroftiana seeds (SMS) in Tibetan medicine for heat-clearing, damp-drying, anti-inflammatory and detoxifying properties, the anti-inflammatory mechanisms of SMS remain insufficiently understood and warrant systematic investigation. This study evaluated the protective effects of an ethanolic SMS extract against lipopolysaccharide (LPS)-induced oxidative stress and inflammation in RAW 264.7 macrophages, with emphasis on the p62/Keap1/Nrf2 signaling pathway. In vitro, the extract exhibited significant DPPH, ABTS and ·OH radical scavenging activities, as well as ferric-reducing antioxidant power, in a clear concentration dependent manner. An inflammatory model was established by stimulating RAW 264.7 cells with LPS, followed by treatment with graded concentrations of the ethanolic SMS extract. The extract significantly reduced LPS-induced nitric oxide production and decreased the secretion of TNF-α, IL-6 and IL-1β, while suppressing iNOS and COX-2 expression at both mRNA and protein levels. In parallel, the extract alleviated oxidative stress, as evidenced by reduced intracellular reactive oxygen species (ROS) and MDA levels, increased antioxidant defenses including SOD, GSH and CAT, and decreased LDH release. At the protein-expression level, SMS treatment was accompanied by differential changes in p62, Keap1, total Nrf2 and HO-1 expression, suggesting that its effects may involve regulatory processes associated with cellular stress and antioxidant defense. Collectively, the ethanolic extract of SMS attenuated LPS-induced inflammatory and oxidative stress responses in RAW 264.7 macrophages. These effects may be associated with the suppression of inflammatory mediator production, reduction in the cellular oxidative stress burden and modulation of proteins involved in cellular stress responses and antioxidant defense. Full article

Background: Conventional tyrosinase (TYR) inhibitors irritate skin and trigger rebound pigmentation, necessitating safer and more effective depigmenting agents. Methods: Biocompatibility was assessed by cell viability. Melanin content and TYR activity were measured spectrophotometrically. Reactive oxygen species (ROS), adenosine triphosphate (ATP), and inflammatory cytokines were detected by fluorescence, luminescence, and ELISA. Western blot and RT-qPCR assessed oxidative stress, inflammatory, and melanogenic targets. Molecular docking simulated Ganoderic Acid A (GAA) interactions with key proteins. Results: GAA exhibits good biocompatibility, inhibits melanin synthesis and TYR activity in B16-F10 cells, and reverses ultraviolet B-induced pigmentation. Mechanistically, GAA restores mitochondrial homeostasis by scavenging ROS, replenishing ATP, activating the nuclear factor erythroid 2-related factor 2 (Nrf2) axis, and inhibiting nuclear factor kappa-B (NF-κB) and cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) to regulate the inflammatory microenvironment. This synergistic regulation inhibits the mitogen-activated protein kinase (MAPK) signaling pathway and down-regulates the microphthalmia-associated transcription factor (MITF) transcriptional network and the expression of TYR, tyrosinase-related protein 1 (TRP-1), and tyrosinase-related protein 2 (TRP-2). Conclusion: GAA eliminates ultraviolet B-induced hyperpigmentation through a multi-target mechanism of mitochondrial repair, inflammation inhibition, and direct binding to tyrosinase, and is a potential natural candidate drug for the treatment of skin diseases. Full article

Reactive oxygen species (ROS) exert dual biological functions in plants. Though they form toxic byproducts of aerobic metabolism, ROS also serve as indispensable secondary messengers that orchestrate stress acclimation programs. For decades, plant physiologists operated under a pervasive assumption that constitutive and non-compartmentalized upregulation of antioxidant capacity would universally enhance abiotic stress tolerance. This long-standing dogma has now been thoroughly overturned. A growing body of evidence shows that sustained, global high antioxidant activity often impairs adaptation rather than helping it. In this review, we replace the simplistic “more antioxidants equal better tolerance” framework with a dynamic model of cellular redox homeostasis. We dissect three interconnected mechanisms though which unrestrained ROS scavenging generates deleterious phenotypic outcomes. First, indiscriminate clearance blunts transient ROS pulses and propagating ROS waves, the core signaling events acquired to trigger systemic acquired acclimation (SAA). Second, continuous antioxidant biosynthesis drains finite carbon skeletons, NADPH, and ATP pools, exacerbating evolutionary growth-defense resource trade-offs. Third, non-specific bulk ROS scavenging erases compartment-specific organellar retrograde signals, which rely on tightly controlled spatial and temporal ROS fluctuations. We concurrently define physiological boundary conditions where robust antioxidant activity remains vital for plant survival under extreme stress. Rather than advocating for the complete suppression of ROS detoxification, our analysis advocates context-dependent fine-tuning of redox signaling networks. We also summarize emerging precision redox monitoring and genetic engineering tools, and outline translational breeding pipelines to develop climate-resilient crops that balance stress survival and yield stability. This work delivers novel conceptual perspectives to advance fundamental plant redox biology. Full article