Search Results (9,589)

Background and Objectives: This study aimed to investigate the anticancer effects and potential synergistic interactions of quercetin (Q) and doxorubicin (Dox) on the MG-63 osteosarcoma (OS) cell line. Specifically, the effects of these agents on cell viability, apoptosis, reactive oxygen species (ROS) generation, antioxidant defense, and the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt1) signaling pathway were evaluated. Material and Methods: MG-63 cells were cultured and treated with varying concentrations of Q and Dox, both individually and in combination (fixed 5:1 molar ratio), for 48 h. Cell viability was assessed using an MTT assay, and IC₅₀ values were calculated. Synergistic effects were analyzed using the Chou–Talalay combination index (CI). Apoptosis was evaluated via Annexin V-FITC/PI staining and caspase-3/7 activity. ROS levels were quantified using DCFH-DA probe, and antioxidant enzymes (SOD, GPx) were measured spectrophotometrically. Gene expression (Runx2, PI3K, Akt1, caspase-3) was analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Results: Q and Dox reduced cell viability in a dose-dependent manner, with IC₅₀ values of 70.3 µM and 1.14 µM, respectively. The combination treatment exhibited synergistic cytotoxicity (CI < 1), especially in the Q50 + Dox5 group (CI = 0.23). Apoptosis was significantly enhanced in the combination group, evidenced by increased Annexin V positivity and caspase-3 activation. ROS levels were markedly elevated, while antioxidant enzyme activities declined. RT-qPCR revealed upregulation of caspase-3 and downregulation of Runx2, PI3K, and Akt1 mRNA levels. Conclusions: The combination of Q and Dox exerts synergistic anticancer effects in MG-63 OS cells by inducing apoptosis, elevating oxidative stress, suppressing antioxidant defense, and inhibiting the PI3K/Akt1 signaling pathway and Runx2 expression. These findings support the potential utility of Q as an adjuvant to enhance Dox efficacy in OS treatment. Full article

Alcohol dependency is a complex and chronic condition that negatively impacts multiple organ systems, including the skin. A key pathological factor in this process is oxidative stress, leading to progressive cellular damage, chronic inflammation, and accelerated cutaneous aging. Alcohol metabolism generates reactive oxygen species (ROS), which overwhelm endogenous antioxidant defenses and contribute to a range of skin alterations, including nonspecific changes such as xerosis, erythema, and wrinkle formation, as well as inflammatory and neoplastic skin disorders. Additionally, alcohol-induced alterations of the skin microbiome may further exacerbate skin barrier dysfunction and inflammatory responses. This review explores the biochemical mechanisms and skin microbiome alterations linking alcohol-induced oxidative stress to skin damage and disease. Furthermore, it evaluates the therapeutic potential of antioxidant-based interventions, both natural and synthetic. Antioxidants may offer protective and regenerative effects by scavenging free radicals, modulating inflammatory responses, and enhancing skin barrier function. The paper aims to provide a comprehensive overview of the molecular and microbial interplay between alcohol, oxidative stress, and skin health, while identifying future directions for targeted antioxidant therapy in individuals with alcohol dependency. Full article

Plants are constantly exposed to environmental stressors such as drought, salinity, and extreme temperatures, which threaten their growth and productivity. To counter these challenges, they employ complex molecular defense systems, including epigenetic modifications that regulate gene expression without altering the underlying DNA sequence. This review comprehensively examines the emerging roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) as central signaling molecules orchestrating epigenetic changes in response to abiotic stress. In addition, biotic factors such as pathogen infection and microbial interactions are considered for their ability to trigger ROS/RNS generation and epigenetic remodeling. It explores how ROS and RNS influence DNA methylation, histone modifications, and small RNA pathways, thereby modulating chromatin structure and stress-responsive gene expression. Mechanistic insights into redox-mediated regulation of DNA methyltransferases, histone acetyltransferases, and microRNA expression are discussed in the context of plant stress resilience. The review also highlights cutting-edge epigenomic technologies such as whole-genome bisulfite sequencing (WGBS), chromatin immunoprecipitation sequencing (ChIP-seq), and small RNA sequencing, which are enabling precise mapping of stress-induced epigenetic landscapes. By integrating redox biology with epigenetics, this work provides a novel framework for engineering climate-resilient crops through the targeted manipulation of stress-responsive epigenomic signatures. Full article

Although platelets have been traditionally thought of to be essential hemostasis mediators, new research shows how important they are for controlling cellular oxidative stress, inflammatory processes, and immunological responses—particularly during major surgery on the abdomen. Perioperative problems are largely caused by the continually changing interaction of inflammatory cytokines, the formation of reactive oxygen species (ROS), and platelet activation. The purpose of this review is to summarize the most recent data regarding the complex function of platelets in abdominal surgery, with an emphasis on how they interact with inflammation and oxidative stress, and to investigate the impact on postoperative therapy and subsequent studies. Recent study data on platelet biology, redox signals, surgical stress, and antiplatelet tactics was reviewed in a systematic manner. Novel tailored therapies, perioperative antiplatelet medication, oxidative biomarkers of interest, and platelet-derived microscopic particles are important themes. In surgical procedures, oxidative stress dramatically increases the reactive capacity of platelets, spurring thromboinflammatory processes that affect cardiac attacks, infection risk, and recovery. A number of biomarkers, including soluble CD40L, thromboxane B2, and sNOX2-derived peptide, showed potential in forecasting results and tailored treatment. Antiplatelet medications are still essential for controlling risk factors for cardiovascular disease, yet using them during surgery necessitates carefully weighing the risks of thrombosis and bleeding. Biomarker-guided therapies, antioxidant adjuncts, and specific platelet inhibitors are examples of evolving tactics. In abdominal procedures, platelets strategically operate at the nexus of oxidative stress, inflammatory processes, and clotting. Improved patient classification, fewer problems, and the creation of individualized surgical care strategies could result from an increased incorporation of platelet-focused tests and therapies into perioperative processes. To improve clinical recommendations, subsequent studies may want to focus on randomized studies, biomarker verification, and using translational approaches. Full article

Air pollution acts as a pervasive oxidative stressor, disrupting global crop production and ecosystem health through the overproduction of reactive oxygen species (ROS). Hazardous pollutants impair critical physiological processes—photosynthesis, respiration, and nutrient uptake—triggering oxidative damage and yield losses. This review synthesizes current knowledge on plant defense mechanisms, emphasizing the integration of enzymatic (SOD, POD, CAT, APX, GPX, GR) and non-enzymatic (polyphenols, glutathione, ascorbate, phytochelatins) antioxidant systems to scavenge ROS and maintain redox homeostasis. We highlight the pivotal roles of transcription factors (MYB, WRKY, NAC) in orchestrating stress-responsive gene networks, alongside MAPK and phytohormone signaling (salicylic acid, jasmonic acid, ethylene), in mitigating oxidative stress. Secondary metabolites (flavonoids, lignin, terpenoids) are examined as biochemical shields against ROS and pollutant toxicity, with evidence from transcriptomic and metabolomic studies revealing their biosynthetic regulation. Furthermore, we explore biotechnological strategies to enhance antioxidant capacity, including overexpression of ROS-scavenging genes (e.g., TaCAT3) and engineering of phenolic pathways. By addressing gaps in understanding combined stress responses, this review provides a roadmap for developing resilient crops through antioxidant-focused interventions, ensuring sustainability in polluted environments. Full article

The intestinal barrier governs organismal health through nutrient absorption, microbial homeostasis, and immune surveillance. While calorie restriction (CR) enhances metabolic health, the molecular mechanisms underlying its beneficial effects on gut integrity remain unclear. Here, we demonstrate that the aryl hydrocarbon receptor (AHR), a conserved xenobiotic sensor and metabolic regulator, is essential for CR-mediated improvements in intestinal function. Using Caenorhabditis elegans (C. elegans), we subjected wild-type (N2) and AHR-deficient strains (CZ2485 and ZG24) to ad libitum feeding (AL), intermittent fasting (IF), or complete food deprivation (FD). In wild-type animals, intermittent fasting markedly reduced intestinal permeability and bacterial burden while enhancing mitochondrial function and reducing reactive oxygen species. Complete food deprivation conferred modest benefits. Remarkably, these protective effects were severely compromised in AHR mutants, which exhibited increased gut leakage, bacterial colonization, and mitochondrial oxidative stress under fasting conditions. These findings establish AHR as a critical mediator of fasting-induced intestinal resilience, revealing a previously unrecognized regulatory axis linking metabolic sensing to gut barrier homeostasis. Our work illuminates fundamental mechanisms through which calorie restriction promotes gastrointestinal health and identifies AHR-dependent pathways as promising therapeutic targets for metabolic and inflammatory distress affecting the gut–systemic interface. Full article

Approximately 90% of liver cancer cases are classified as hepatocellular carcinomas (HCCs), with chemotherapy and immunotherapy being the most recommended treatment options. While conventional chemotherapy specifically targets rapidly dividing cancer cells, it can also impact on healthy cells that are proliferating quickly. This collateral damage to healthy cells, along with the potential for cancer cells to develop resistance, presents significant challenges for conventional chemotherapy in liver cancer patients. Hepatic artery infusion of chemotherapy (HAIC) generally leads to reduced toxicity and fewer side effects. The process of catheter insertion is usually performed under local anesthesia, with lidocaine being the preferred choice to combine with various chemotherapeutics in HCC treatment. In our study, we explored the effects of repurposing lidocaine in combination with cisplatin or 5-fluorouracil (5-FU) on two HCC cell lines, HepG2 and Hep3B. Our cytotoxicity analysis revealed that lidocaine functions as a chemosensitizer for cisplatin and 5-FU in both HepG2 and Hep3B cells. Specifically, we observed an increase in the subG1 population and a reduction in cytosolic reactive oxygen species in cisplatin- or 5-FU-treated HepG2 and Hep3B cells. Interestingly, lidocaine selectively decreased the reduced/oxidized glutathione ratio in cisplatin- or 5-FU-treated HepG2 cells but not in Hep3B cells. Furthermore, lidocaine induced endoplasmic reticulum stress, apoptosis, mitochondrial membrane depolarization, lipid peroxidation, and autophagy while suppressing cellular proliferation HepG2 and Hep3B cells. In conclusion, our study demonstrates the synergistic potential of combining lidocaine with cisplatin or 5-FU for the treatment of HCC, indicating that lidocaine may serve as an effective chemosensitizer. These findings highlight a new clinical advantage of using repurposing lidocaine as a chemosensitizer in the current HAIC procedure, suggesting that this combination warrants further exploration through rigorous clinical trials. In the future, we can better optimize therapeutic regimens, potentially leading to improved patient outcomes in HCCs. Full article

The utilization of saline–alkali land for rice cultivation is critical for global food security. However, most existing studies on rice salt tolerance focus on the seedling stage, with limited insights into tolerance mechanisms during reproductive growth, particularly at the panicle initiation stage (PI). Leveraging precision salinity-control facilities, this study imposed four salt stress gradients (0, 3, 5, and 7‰) to dissect the differential response mechanisms of six rice varieties (YXYZ: Yuxiangyouzhan, JLY3261: Jingliangyou3261, SLY91: Shuangliangyou91, SLY138: Shuangliangyou138, HLYYHSM: Hualiangyouyuehesimiao, and SLY11:Shuangliangyou111) during PI. The results revealed that increasing salinity significantly reduced tiller number (13.14–68.04%), leaf area index (18.58–57.99%), canopy light interception rate (11.91–44.08%), and net photosynthetic rate (2.63–52.42%) (p < 0.001), accompanied by reactive oxygen species (ROS)-induced membrane lipid peroxidation. Integrative analysis of field phenotypic and physiological indices revealed distinct adaptation strategies: JLY3261 rapidly activated antioxidant enzymes under 3‰ salinity, alleviating lipid peroxidation (no significant difference in H₂O₂ or malondialdehyde content compared to 0‰ salinity) and maintaining tillering and aboveground biomass. SLY91 tolerated 7‰ salinity via CAT/POD-mediated lipid peroxide degradation, with H₂O₂ and malondialdehyde contents increasing initially but decreasing with escalating stress. These findings highlight genotype-specific antioxidant strategies underlying salt-tolerance mechanisms and the critical need for integrating phenomics–physiological assessments at reproductive stages into salt-tolerance breeding pipelines. Full article

Tea is one of the most consumed beverages in the world, belonging to the category of compounds known as tannins and flavonoids. One of the polyphenols found in large amounts in green tea leaves (Camellia sinensis) is epigallocatechin-3-O-gallate (EGCG). Though EGCG has shown some pharmacological effects, to date, it has not been utilised as a therapeutic agent. This is attributed to the fact that EGCG lacks adequate stability, and it is known to degrade through epimerization or auto-oxidation processes, especially when it is exposed to light, temperature fluctuations, some pH values, or the presence of oxygen. Consuming green tea with EGCG can alleviate the effects of bone diseases, such as osteoporosis, and support faster bone regeneration in the case of fractures. Therefore, this review focuses on the current state of research, highlighting the effects of EGCG on bone biology, such as enhancing osteoblast differentiation, promoting bone mineralisation, improving bone microarchitecture, and inhibiting osteoclastogenesis through the modulation of the RANK/RANKL/OPG pathway. Additionally, EGCG exerts antioxidant, anti-inflammatory, and dose-dependent effects on bone cells. It also downregulates inflammatory markers (TNF-α, IL-1β, and COX-2) and reduces oxidative stress via the inhibition of reactive oxygen species generation and the activation of protective signalling pathways (e.g., MAPK and NF-κB). Studies in animal models confirm that EGCG supplementation leads to increased bone mass and strength. These findings collectively support the further exploration of EGCG as an adjunct in the treatment and prevention of metabolic bone diseases. The authors aim to present the relationship between EGCG and bone health, highlighting issues for future research and clinical applications. Full article

Creole goats have adapted to the harsh Andean environment, yet the physiological impacts of high-altitude production systems remain underexplored. This study assessed seasonal and dietary influences on the hematological and biochemical profiles of 45 Creole goats in the Peruvian Andes. The animals were assigned to three diets: D1 (grazing), D2 (grazing + 2000 g hay), and D3 (grazing + 400 g concentrate), across rainy and dry seasons. Biweekly blood sampling measured urea, cholesterol, total protein, albumin, ALP, ALT, WBCL, NeuP, LymP, HGB, and MCV. Season exerted the strongest influence (p < 0.001), with modest dietary effects and a consistent effect of sampling time. Urea, total protein, and albumin increased during the rainy season, though only urea responded significantly to diet. Leukocytosis rose in the dry season and with higher-protein diets, suggesting heightened immune activation under environmental stress. Hemoglobin peaked in the rainy season and early sampling, indicating better oxygenation. MCV and body weight were higher in the dry season, with weight unaffected by diet. These results underscore the complex interplay of environmental and nutritional factors in shaping goat physiology at high altitudes, emphasizing the importance of dynamic modeling in sustainable Andean livestock systems. Full article

Nanoceria is a multifaceted enzyme-like catalyst of ROS-mediated (reactive oxygen species) reactions, which results in its multiple biomedical applications. Biodegradable polysaccharide coatings improve biocompatibility, while the effects of these coatings on the ROS-related activity of nanoceria in cells need thorough studies. Here, we used human embryonic lung fibroblasts to study the effects of maltodextrin and chitosan coatings on cellular oxidative metabolism of nanoceria by examining cell viability, mitochondrial potential, accumulation of nanoparticles in cells, intracellular ROS, expression of NOX4 (NADPH oxidase 4), NRF2 (nuclear factor erythroid 2-related factor 2), NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), and STAT3 (signal transducer and activator of transcription 3) proteins as well as the expression of biomarkers of DNA damage/repair, cell proliferation, and autophagy. Both types of polysaccharide-coated nanoceria were non-toxic up to millimolar concentrations. For maltodextrin-coated nano-CeO₂, in contrast to bare nanoparticles, there was no oxidative DNA damage/repair with moderate activation of NOX4 expression. Like bare nanoceria, maltodextrin-coated nanoparticles demonstrate the proliferative impact and do not activate autophagy. However, maltodextrin-coated nanoparticles have an activating impact on mitochondrial potential and the NF-κB pathway. Chitosan-coated nanoceria causes short-term intracellular oxidative stress, activation of the expression of NOX4, STAT3, and NRF2, oxidative DNA damage, and double-strand breaks accompanied by activation of DNA repair systems. In contrast to maltodextrin-coated nanoparticles, chitosan-coated nanoceria inhibits the NF-κB pathway and activates autophagy. These findings would be useful in the development of advanced nanoceria-based pharmaceuticals and contribute to the understanding of the biochemical properties of nanoceria as a modulator of ROS-dependent signaling pathways. Full article

Hypoxia represents a critical environmental stressor in aquaculture, significantly disrupting aquatic organisms’ physiological homeostasis and thereby constraining the sustainable development of aquaculture industries. To elucidate the mechanisms underlying hypoxia-induced metabolic regulation in aquatic species, this study employed hybrid yellow catfish (Pelteobagrus vachelli ♀ × Leiocassis longirostris ♂) as a model organism to systematically investigate the multidimensional physiological responses in brain, liver, and muscle tissues under hypoxia (0.7 mg/L) and reoxygenation (7.0 mg/L) conditions. Through qRT-PCR and enzymatic activity analyses, we comprehensively assessed molecular alterations associated with oxygen sensing (HIF-1α gene), respiratory metabolism (PFKL, HK1, PK, CS, and LDHA genes and corresponding enzyme activities), oxidative stress (SOD1, SOD2, GSH-PX, and CAT genes, along with LPO, MDA, PCO, T-SOD, GSH-PX, and CAT levels), apoptosis (Caspase-3, Bax/Bcl-2), inflammatory response (IL-1β, IKKβ), and mitochondrial function (COXIV, PGC-1α, ATP5A1). Key findings demonstrated pronounced HIF-1α activation across all examined tissues. Hepatic tissues exhibited adaptive metabolic reprogramming from aerobic to anaerobic metabolism, whereas cerebral tissues displayed suppressed anaerobic glycolysis during prolonged hypoxia, and muscular tissues manifested concurrent inhibition of both glycolytic and aerobic metabolic pathways. Notably, skeletal muscle exhibited marked oxidative stress accompanied by mitochondrial dysfunction, exacerbated inflammation, and apoptosis activation during hypoxia/reoxygenation cycles. This study delineates tissue-specific adaptive mechanisms to hypoxia in yellow catfish, providing theoretical foundations for both piscine hypoxia physiology research and aquaculture practices. Full article

By introducing oxygen doping, the structure of an AlCrNbSiTiN coating was optimized, and its high-temperature oxidation resistance was improved. As the oxygen content incorporated increases, the coating changes from an FCC structure to an amorphous or spinel structure. Meanwhile, stress relaxation occurred, and the hardness of the coating dropped to 12 gpa. Oxygen-doped coatings exhibit excellent oxidation resistance; this is especially the case for oxidized coatings, whose structure remains stable up to 900 °C in an oxidizing environment. Full article

Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity. Full article

Inflammatory bowel disease (IBD) is characterized by oxidative stress imbalance and intestinal barrier disruption. Reducing excessive ROS has become a promising therapeutic strategy. Compared with conventional polyphenols, nanomaterials offer greater stability and bioavailability for ROS scavenging. Here, ellagic acid (EA) was converted into uniform nanoparticles (EAs) with reactive oxygen scavenging capacity through horseradish peroxidase (HRP)-mediated oxidative polymerization and subsequently encapsulated in the anti-gastric acid hydrogel F-DP to obtain the hybrid system F-DP@EAs. EAs reduced ROS, MDA, NO, IL-1β, and TNF-α levels in vitro, while increasing IL-4 and IL-10 expression, thus alleviating inflammation. Herein, F-DP@EAs prolonged intestinal retention time and exerted superior protective effects in the DSS-induced colitis model. Oral F-DP@EAs lowered DAI, preserved colon length, increased glutathione (GSH) and superoxide dismutase (SOD), decreased NO and MDA, restored zonula occludens-1 (ZO-1), and reduced mucosal lesions. These findings demonstrate that combining nanoparticle and hydrogel technologies markedly enhances the preventive and protective efficacy of EA, highlighting F-DP@EAs as a promising candidate for future IBD therapy. Full article