Antioxidants最新文献

{"title":"Effect of the Rate of Glucose Consumption on the Total Peroxyl Radical Trapping Antioxidant Potential (TRAP) of Plasma in Overweight Men and Women: A Randomized Trial.","authors":"Shannan M Grant, Thomas M S Wolever, Alexandra Thompson, Laura Chiavaroli, Maxine Seider, Antonia Harvey, Megan Gray, Pauline Darling, Deborah O'Connor, Robert G Josse, Kazimiera A Mizier-Barre, David Kitts, Douglas Edward Barre","doi":"10.3390/antiox15040512","DOIUrl":"10.3390/antiox15040512","url":null,"abstract":"<p><p>Low glycemic-index foods may reduce postprandial oxidative stress by reducing postprandial glucose excursions, but the evidence for this is limited by dietary confounders. To determine whether reducing postprandial glucose per se reduces postprandial oxidative stress, overnight-fasted participants (BMI 25.0-39.9 kg/m², n = 18) consumed four test meals in random order: 75 g dextrose solution (Dex) within 5 min (bolus/noC), Dex slowly over 3.25 h (sipping/noC), bolus with 1 g vitamin C (bolus/C) and sipping with 1 g vitamin C (sipping/C). Venous blood was taken at intervals over 6 h; a standard lunch was consumed at 4 h. Sipping flattened postprandial glucose and insulin and reduced free fatty acid rebound compared to bolus (<i>p</i> < 0.05). Vitamin C raised serum vitamin C from ~20 to ~55 μmol/L. The total peroxyl radical trapping antioxidant potential (TRAP) increments differed after lunch, with a main effect of vitamin C at 5 h (mean ± SEM; C 70 ± 23 vs. noC -29 ± 27; <i>p</i> = 0.016) and main effects of rate (sipping 57 ± 25 vs. bolus -71 ± 28; <i>p</i> = 0.0002) and vitamin C (C 58 ± 25 vs. noC -73 ± 28; <i>p</i> = 0.0003) at 6 h. By multiple regression analysis, the TRAP area under the curve (AUC) was positively associated with the insulin AUC (<i>p</i> < 0.001) and negatively with the glucose and vitamin C AUCs (<i>p</i> < 0.05). The oxidized LDL increments were higher 6 h after sipping than bolus (7 ± 7 vs. -20 ± 7, <i>p</i> = 0.005). The oxidized LDL AUC was negatively associated with the TRAP AUC (<i>p</i> < 0.001). These results support the hypothesis that reducing postprandial glucose reduces postprandial oxidative stress.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.","authors":"Antonella Tramutola, Chiara Lanzillotta, Fabio Di Domenico, Eugenio Barone, Marzia Perluigi","doi":"10.3390/antiox15040520","DOIUrl":"10.3390/antiox15040520","url":null,"abstract":"<p><p>Down syndrome (DS), caused by trisomy 21, is the most prevalent genetic condition associated with accelerated aging and near-universal development of early-onset Alzheimer's disease (AD). Beyond gene-dosage imbalance, trisomy 21 induces widespread transcriptional, metabolic, and proteomic remodeling that establishes a chronic state of proteotoxic and oxidative stress from early development. Increasing evidence identifies DS as a disorder of proteostasis network failure, in which sustained translational pressure, redox disequilibrium, and degradation pathway insufficiency progressively erode cellular resilience. In the DS brain, persistent endoplasmic reticulum stress with PERK-dominant signaling, mitochondrial dysfunction characterized by oxidative phosphorylation deficits and excessive reactive oxygen species production, and impaired antioxidant responses create a highly vulnerable intracellular environment. Concomitantly, degradation systems become compromised: proteasomal catalytic activity declines, ubiquitin-dependent signaling is remodeled, and chronic mTOR hyperactivation suppresses autophagic and mitophagic flux. The coordinated impairment of the ubiquitin-proteasome system and autophagy establish a feed-forward cycle of proteotoxic accumulation and redox amplification. Within this framework, Alzheimer-like neuropathology in DS emerges not solely from amyloid precursor protein triplication but as the late manifestation of decades-long proteostasis exhaustion. Therapeutic strategies aimed at restoring global proteostasis and redox balance may therefore represent a more effective systems-level approach to mitigating neurodegeneration in DS.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Absolute Quantitation of Phenolic Compounds in Olive Oil for Health Claim Recognition.","authors":"Ana Castillo-Luna, Feliciano Priego-Capote","doi":"10.3390/antiox15040511","DOIUrl":"10.3390/antiox15040511","url":null,"abstract":"<p><p>The European Regulation (UE) 432/2012 includes a specific health claim for olive-oil-associated with its phenolic content, which is based on its protective role against lipid oxidation in the blood. To make use of the health claim, olive oil must have a minimum concentration in phenolic compounds of 250 mg/kg. Reviewing the health claim, the phenolic compounds referred to are the secoiridoid derivatives of hydroxytyrosol and tyrosol. A method based on absolute quantification of phenolic compounds in olive oil is proposed for the recognition of the health claim. The method involves liquid-liquid extraction with a 1:8 (<i>v</i>/<i>v</i>) oil:extract ratio to avoid saturation of the extract in oils with a higher phenolic content and its subsequent determination through LC-MS/MS in multiple reaction monitoring (MRM) mode, the gold standard technique in many application fields because of its analytical features. The optimized method was applied to a set of 100 extra virgin olive oils (EVOOs), and the results obtained were compared with the classic Folin-Ciocalteu method. The comparison between the two methods showed that the classic method is a non-selective method that can be affected by many interferences and that the Folin method underestimates the real phenolic content.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Atherogenic Actions of Pomegranate Polyphenol Punicalagin and Its Metabolites: In Vitro Effects on Vascular Cells and In Vivo Atheroprotection by Urolithin A via Anti-Inflammatory and Plaque-Stabilising Mechanisms.","authors":"Sulaiman Alalawi, Daniah Rifqi, Alaa Alhamadi, Reem Alotibi, Fahad Alradi, Nouf Alshehri, Yee-Hung Chan, Jing Chen, Faizah Albalawi, Sarab Taha, Nabras Al-Mahrami, Irina A Guschina, Timothy R Hughes, Dipak P Ramji","doi":"10.3390/antiox15040507","DOIUrl":"10.3390/antiox15040507","url":null,"abstract":"<p><p>Nutraceuticals are emerging as promising agents for the prevention and treatment of atherosclerosis, particularly in light of the limitations associated with current pharmacotherapies. Pomegranate-derived polyphenols, especially punicalagin (PC), possess multiple cardioprotective properties. However, their direct biological effects are constrained by poor absorption and low bioavailability. Instead, many of their actions are mediated by gut microbiota-derived metabolites known as urolithins. Despite this, the roles of PC and its metabolites in atherosclerosis remain inadequately defined. The objective of this study was to investigate the anti-atherogenic effects and underlying mechanisms of PC and its major metabolites-ellagic acid and urolithins A, B, C, and D-using in vitro and in vivo approaches. In vitro, these compounds broadly inhibited key pro-atherogenic processes in macrophages and endothelial cells, including reactive oxygen species production and inflammatory gene expression, with notable metabolite-specific differences. Urolithin A (UA), identified as the most effective compound, was further evaluated in LDL receptor-deficient mice fed a high-fat diet. UA supplementation improved peripheral blood immune cell profile, reduced atherosclerotic plaque burden and inflammation, and enhanced markers of plaque stability. RNA sequencing of the thoracic aorta revealed key molecular pathways underlying the protective actions of UA. Collectively, these findings highlight the therapeutic potential of PC-derived metabolites, particularly UA, in combating atherosclerosis and support the need for future human clinical studies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Attenuates H₂O₂-Induced Oxidative Stress by Restoring Redox Balance, Mitochondrial Integrity and Reducing Apoptosis in Buffalo Fibroblasts.","authors":"Priya Dahiya, Manu Mangal, Srishti Bhatia, Neha Sharma, Ashish Sindhu, Bhavya Maggo, Meeti Punetha, Renu Bala, Pradeep Kumar, Dharmendra Kumar","doi":"10.3390/antiox15040508","DOIUrl":"10.3390/antiox15040508","url":null,"abstract":"<p><p>Oxidative stress critically affects cellular viability and function under in vitro culture conditions, often compromising physiological integrity of somatic cells used in livestock biotechnology. This study aimed to investigate hydrogen peroxide (H₂O₂)-induced oxidative stress in buffalo fibroblasts and evaluated the cytoprotective effects of melatonin, focusing on redox homeostasis, mitochondrial function, apoptosis, and antioxidant defence. Fibroblasts were exposed to graded concentrations of H₂O₂ (100-1000 µM) for 2 h, followed by treatment for 72 h in culture media with and without melatonin (10^-9 M). Oxidative stress markers, including GSSG/GSH ratio, ROS generation, mitochondrial membrane potential (MMP), and apoptosis, were assessed using flow cytometry and biochemical assays, while antioxidant (GPx, SOD, CAT) and apoptotic (BAX, Caspase 9) gene expression was analyzed by qPCR. H₂O₂ exposure induced a dose-dependent increase in oxidative stress, evidenced by elevated ROS, redox imbalance, mitochondrial depolarization, and enhanced apoptosis. Severe oxidative damage was observed at higher H₂O₂ (500-1000 µM) concentrations. Melatonin (MT) significantly (<i>p</i> ≤ 0.05) alleviated oxidative stress under mild to moderate conditions (100-200 µM H₂O₂) by restoring redox homeostasis, preserving mitochondrial integrity, suppressing ROS accumulation, enhancing antioxidant defence, and reducing apoptosis. However, its protective efficacy was lost under severe oxidative stress, indicating a defined redox threshold beyond which cellular damage becomes irreversible. These findings suggest that melatonin exerts cytoprotective effect against oxidative stress within a limited oxidative window and provide mechanistic insights for improving fibroblasts culture systems in livestock biotechnology and regenerative applications.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant, Anti-Cholinesterase, and Neuroprotective Properties of <i>Morus alba</i> and <i>Morus nigra</i> Extracts.","authors":"Emanuela Nani Pohrib, Andreia Corciova, Oana Cioanca, Lucian Hritcu, Monica Hancianu, Andreea-Maria Mitran, Ana Flavia Burlec, Alexandra-Mara Cimpanu, Crina-Maria Isac, Riana Huzum, Ecaterina Danu, Cornelia Mircea","doi":"10.3390/antiox15040510","DOIUrl":"10.3390/antiox15040510","url":null,"abstract":"<p><p>The <i>Morus</i> genus comprises several tree species whose fruits are used in human nutrition, while the leaves and roots are used in traditional medicine. The aim of this study was to highlight the antioxidant, cholinesterase inhibitory, and neuroprotective effects of hydroalcoholic extracts from <i>Morus alba</i> (MAE) and <i>Morus nigra</i> (MNE) leaves. RP-UHPLC-PDA analysis of extracts revealed the presence of polyphenols in higher quantities in MNE extract compared to MAE. Both extracts demonstrated antioxidant properties in the hydroxyl radical scavenging and lipid peroxidation inhibition assays. MNE exhibited a superior antioxidant capacity compared to MAE; the IC₅₀ values for the inhibition of plasma lipid oxidation assay were 25.31 ± 2.54 µg/mL for MNE and 29.85 ± 0.97 µg/mL for MAE. Both extracts showed cholinesterase inhibitory activity. The IC₅₀ values for acetylcholinesterase inhibition were 24.34 ± 0.86 µg/mL for MNE and 46.87 ± 2.16 µg/mL for MAE. The inhibitory potency of MNE was comparable to that of galantamine, which was used as standard. Both extracts reversed, in a dose-dependent manner, the scopolamine-induced cognitive impairment and behavioural alterations in scopolamine-treated zebrafish (<i>Danio rerio</i>) as evaluated by the Y-maze test, novel tank diving test, and novel object recognition test.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13113132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol and Redox Regulation in Cardiovascular Disease Across the Life Course: Mechanistic and Translational Perspectives.","authors":"Chien-Ning Hsu, You-Lin Tain","doi":"10.3390/antiox15040509","DOIUrl":"10.3390/antiox15040509","url":null,"abstract":"<p><p>Resveratrol (RSV), a bioactive polyphenol, has emerged as a pleiotropic modulator within the integrated pathophysiology of cardiovascular disease (CVD) across the life course. Effective CVD management requires a transition from organ-centric frameworks to systems-level models that acknowledge dynamic crosstalk among metabolic, renal, and cardiovascular networks. Oxidative stress constitutes a central unifying axis in this interconnected biology, propagating cross-organ injury from early developmental stages onward. Mechanistically, RSV acts as a redox-responsive gene regulator by activating the Nrf2-ARE pathway, restoring nitric oxide bioavailability, and orchestrating SIRT1, AMPK, and NF-κB signaling to recalibrate mitochondrial function, inflammatory tone, and endothelial integrity. Within the Developmental Origins of Health and Disease (DOHaD) paradigm, RSV exhibits reprogramming potential that attenuates the intergenerational transmission of hypertension, kidney disease, and metabolic dysfunction. Although clinical translation is constrained by limited bioavailability and rapid metabolism, advanced delivery systems and artificial intelligence-enabled optimization strategies provide promising avenues to enhance therapeutic precision and scalability. This narrative review integrates mechanistic and translational insights to position RSV as a systems-oriented life-course intervention with sustained and intergenerational relevance in CVD.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterogeneity, Measurement, and Clinical Implications of Oxygenation, Cell Signaling, and Redox Biology in Glioblastoma and Adult Diffuse Gliomas, with Context from Other Brain Tumors.","authors":"Arabinda Das, Julian E Bailes, Ann Barlow, Daniil P Aksenov","doi":"10.3390/antiox15040505","DOIUrl":"10.3390/antiox15040505","url":null,"abstract":"<p><p>Tumor oxygenation is a key determinant of cancer biology and treatment response, correlating with angiogenesis, recurrence, and malignant progression. Hypoxia is a defining feature of glioblastoma (GBM) and adult diffuse gliomas, generating low-oxygen niches that promote invasion, stem-like states, immune suppression, and resistance to radiotherapy and temozolomide, contributing to poor outcomes. Measuring tissue partial pressure of oxygen (pO₂) and mapping its spatial heterogeneity can, therefore, inform mechanistic understanding and therapeutic development, including hypoxia-activated prodrugs, hypoxia-responsive gene therapy, and optimized radiotherapy planning. Although direct pO₂ assessment is challenging, invasive probes and multimodal imaging can characterize regional hypoxia pre-operatively, support patient stratification, monitor treatment effects, and improve outcome prediction. This review summarizes oxygen dynamics in GBM; analyzes causes of hypoxia (rapid growth outpacing supply, diffusion-limited hypoxia, and abnormal/chaotic vasculature); compares methods to quantify oxygenation from direct measurements to noninvasive imaging surrogates; and evaluates preclinical and clinical strategies that target hypoxia to enhance standard therapy, including barriers to translation. We further integrate oxygenation with cell signaling and redox biology: oxygen gradients are transduced via hypoxia-inducible factor programs and redox-sensitive pathways (NRF2/KEAP1, NOX-derived ROS, nitric oxide/S-nitrosylation, and sulfur metabolic routes), shaping mesenchymal-like transitions and cell-death programs such as ferroptosis. Framing oxygenation as both a microenvironmental and redox-signaling variable positions oxygen imaging as an entry point to biomarker-guided therapies that exploit oxidative vulnerabilities.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review of Therapeutic Potential of Coenzyme Q10 in Ophthalmology: Focus on Age-Related Macular Degeneration, Glaucoma, and Retinitis Pigmentosa.","authors":"Michał Wiciński, Anna Fajkiel-Madajczyk, Zuzanna Kurant, Łukasz Rzepiński, Maciej Słupski","doi":"10.3390/antiox15040506","DOIUrl":"10.3390/antiox15040506","url":null,"abstract":"<p><p>Coenzyme Q10 (CoQ10), a natural antioxidant produced by the human body, has strong anti-inflammatory properties, reduces oxidative stress, and improves mitochondrial function. It is also known for its strong neuroprotective effects. With age, endogenously produced CoQ10 levels decline, contributing to the development of chronic diseases, including eye disorders. Irreversible ocular diseases that result in blindness present a significant challenge in contemporary medicine, as no fully effective cure exists; current treatments primarily aim to decelerate disease progression, manage symptoms, and preserve residual vision. Our study reviews research on the use of CoQ10 in eye diseases like age-related macular degeneration (AMD), retinitis pigmentosa (RP), and glaucoma, which can cause permanent vision loss and are linked to oxidative stress and mitochondrial dysfunction. This article explores whether CoQ10 can be a safe and effective addition to treatment for these conditions. We also outline directions for future research and explain how CoQ10 functions in the studies discussed in this review.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13112934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin Attenuates Oxidative Stress and Immune Inflammation via Modulating Heme and ROS Pathways in Rats Fed Protein-Oxidized Soybean Meal.","authors":"Zhiyong Wang, Peng Wang, Yanmin Zhou, Leli Wang, Su Zhuang","doi":"10.3390/antiox15040504","DOIUrl":"10.3390/antiox15040504","url":null,"abstract":"<p><p>Dietary protein oxidation impairs animal health, yet effective interventions remain limited. This study investigated whether quercetin (Q) supplementation protects against protein-oxidized soybean meal (OS)-induced oxidative stress and inflammatory injury in rats. A 2 × 2 factorial experiment was conducted with 48 three-week-old Sprague-Dawley rats randomly assigned to four dietary treatments (<i>n</i> = 12): fresh soybean meal (FS), FS + 400 mg/kg Q, OS, and OS + 400 mg/kg Q for 28 days. Serum biochemistry, intestinal and hepatic histology, antioxidant status, inflammatory markers, and transcriptomic pathways were analyzed. As a result, OS feeding elevated serum glucose and urea nitrogen, induced duodenal, jejunal and hepatic lesions, reduced total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px) activity, glutathione (GSH) level, increased reactive oxygen species (ROS) and malondialdehyde (MDA) content (<i>p</i> < 0.05), and increased IgG and IL-6 levels (<i>p</i> < 0.05). Transcriptomic analysis revealed upregulation of heme biosynthesis and ROS synthesis pathways in jejunum and liver (<i>p</i> < 0.05). Q supplementation mitigated these adverse effects by improving antioxidant status, reducing inflammatory lesions, downregulating heme and ROS pathways, and normalizing the expression of key genes (<i>Ccl20</i>, <i>RT1-M2</i>) and protein (Ccl20) in jejunum (<i>p</i> < 0.05), and key genes (<i>Duox1</i>, <i>Cyp4a2</i>) and protein (Duox1) in liver (<i>p</i> < 0.05). These findings demonstrate that Q alleviates OS-induced oxidative stress, inflammation, and tissue damage through the modulation of heme and ROS pathways.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"15 4","pages":""},"PeriodicalIF":6.6,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13112963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}