Antioxidants最新文献

{"title":"Antioxidant Capacity and Disease Resistance Enhanced by Dietary D-Glucuronolactone Supplementation in Chinese Soft-Shelled Turtles (<i>Pelodiscus sinensis</i>).","authors":"Tong Zhou, Wenyi Wu, Mingyang Xue, Yong Zhou, Hongwei Liang, Wei Liu","doi":"10.3390/antiox14050534","DOIUrl":"10.3390/antiox14050534","url":null,"abstract":"<p><p>D-glucuronolactone (DGL), a hepatoprotective compound widely used in clinical and energy products, was evaluated for its effects on Chinese soft-shelled turtles (<i>Pelodiscus sinensis</i>) through an 8-week feeding trial with dietary supplementation (0, 200, and 400 mg kg^-1). DGL did not alter survival or feed intake, but induced dose-dependent growth improvements, including increased final body weight, weight gain rate, specific growth rate, and muscle/liver glycogen, alongside reduced feed conversion ratio and muscle and liver fat. Serum analysis showed decreased activities of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and reduced low-density lipoprotein cholesterol, total cholesterol, and triacylglycerols. Antioxidant indices revealed elevated catalase and superoxide dismutase (SOD) activities in serum and intestine, coupled with reduced malondialdehyde, though hepatic SOD activity declined. Histologically, 400 mg kg^-1 DGL alleviated liver lesions without impacting intestinal morphology. Molecular analyses demonstrated upregulated muscle <i>mTOR</i> signaling genes (<i>mTOR</i>, <i>IGF1</i>, <i>S6K1</i>) but downregulated hepatic/intestinal <i>mTOR</i> and <i>IGF1</i> expression. DGL also suppressed inflammatory cytokines (<i>TNF-α</i>, <i>IL-1β</i>, <i>IL-10</i>) in liver and intestine. Challenge tests with <i>Aeromonas hydrophila</i> confirmed the enhanced disease resistance in DGL-supplemented turtles. These findings highlight DGL's potential as a nutritional strategy to enhance growth, antioxidant capacity, and health in intensive turtle farming.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155688","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":"A Highly Potent Apomorphine Derivative Enhancing Neurite Outgrowth via Nrf2 Activation.","authors":"Tamaki Ishima, Hitoshi Osaka, Ryozo Nagai, Kenichi Aizawa","doi":"10.3390/antiox14050537","DOIUrl":"10.3390/antiox14050537","url":null,"abstract":"<p><p>Apomorphine (APO), a dopamine agonist, activates nuclear factor erythroid 2-related factor 2 (Nrf2) and exerts antioxidant effects, making it a promising candidate for neuroprotection against oxidative stress. This study evaluated neuroplasticity-enhancing properties of newly synthesized APO derivatives, focusing on their ability to promote neurite outgrowth in PC12 cells under nerve growth factor (NGF) stimulation. D55, an APO derivative, retains the hydroxyl group at APO's 11th position while substituting the 10th with an ethoxy group. D55 exhibited the highest potency (EC₅₀ = 0.5661 nM), significantly enhancing neurite outgrowth. APO demonstrated the highest efficacy (Emax ~10-fold increase), while edaravone (Eda) required higher concentrations (EC₅₀ = 22.5 nM) for moderate effects (Emax ~4-fold increase). D30, in which the 11th hydroxyl was replaced with a methoxy group, had no effect. Neurite outgrowth-promoting effects of APO, D55, and Eda were significantly attenuated by Nrf2 siRNA knockdown, confirming that their neuroplasticity effects are Nrf2-mediated. These findings confirm that D55 is a highly potent Nrf2-activating compound with strong neuroprotective potential, providing new insights into its therapeutic applications for neurodegenerative diseases associated with oxidative stress.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155607","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":"Improvement of the Structure and Antioxidant Activity of Protein-Polyphenol Complexes in Barley Malts Using Roasting Methods.","authors":"Guozhi Wu, Huiting Lin, Yongsheng Chen","doi":"10.3390/antiox14050538","DOIUrl":"10.3390/antiox14050538","url":null,"abstract":"<p><p>Proteins and polyphenols are important components in barley malt. During the roasting process of barley malt, proteins and polyphenols interact and influence each other, ultimately altering the nutritional profile and functional properties of barley malt. In this research, polyphenol-free proteins and protein-polyphenol complexes were extracted from barley malt subjected to varying degrees of roasting. The antioxidant activity of protein-polyphenol complexes was assessed by ABTS, FRAP, and ORAC assays. The structural characteristics of the proteins were examined through UV, FL, CD, FTIR, and SEM. We found that roasting enhances the solubility of globulin, prolamin, and glutenin and facilitates the binding of these proteins with polyphenols. Conversely, the impact of roasting on albumin exhibits a trend opposite to that observed in the other three proteins. The antioxidant activity of protein-polyphenol complexes was significantly higher than that of polyphenol-free proteins. Additionally, the microenvironment of the amino acid residues of the four proteins exhibited increased polarity following the roasting process, and the structural conformation of albumin, globulin, and glutelin transitioned from an ordered to a disordered state. Our results indicate that roasting enhances the antioxidant activity of protein-polyphenol complexes by altering the secondary and tertiary structures of these proteins, thereby exposing more hydrophobic side-chain groups inside the proteins and offering more binding sites for polyphenols.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155763","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":"Time Course of Plasma Proteomic and Oxylipin Changes Induced by LPS Challenge and Modulated by Antioxidant Supplementation in a Randomized Controlled Trial.","authors":"Gerhard Hagn, Andrea Bileck, Thomas Mohr, Doreen Schmidl, David M Baron, Bernd Jilma, Leopold Schmetterer, Gerhard Garhöfer, Christopher Gerner","doi":"10.3390/antiox14050536","DOIUrl":"10.3390/antiox14050536","url":null,"abstract":"<p><p>Systemic molecular responses to pathogen-associated molecular patterns and their modulation by antioxidants are poorly understood in humans. Here, we present a two-stage clinical interventional study in healthy humans challenged with lipopolysaccharide. In the first step, the kinetics of inflammatory modulators within 8 h were investigated by plasma proteomics and lipidomics. In a second step, the effects of a placebo-controlled antioxidant intervention on the individual responses prior to another lipopolysaccharide challenge were determined. Plasma proteomics revealed an early involvement of the endothelium and platelets, followed by the induction of liver-derived acute phase proteins and an innate immune cell response. Untargeted lipidomics revealed an early release of fatty acids and taurocholic acid, followed by complex regulatory events exerted by oxylipins. The consistent lipopolysaccharide-induced downregulation of lysophospholipids suggested the involvement of the Lands cycle, and the downregulation of deoxycholic acid reinforced emerging links between the inflammasome and bile acids. Groups of molecules with similar kinetics to lipopolysaccharide challenge were observed to share precursors, synthesizing enzymes or cellular origin. Dietary antioxidant supplementation prior to lipopolysaccharide challenge had no detectable effect on protein kinetics but significantly downregulated pro-inflammatory sphingosine-1-phosphate and increased levels of oxylipins, 20-HEPE, and 22-HDoHE, which have been described to facilitate the resolution of inflammation. The present study identified a complex network of lipid mediators deregulated in plasma upon lipopolysaccharide challenge and highlighted the role of platelets, endothelial cells, and erythrocytes as potential inflammatory modulators. While dietary antioxidant supplementation hardly affected the initiation of inflammation, it may exert its effects supporting the resolution of inflammation.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155812","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":"Extracellular Vesicles as Epigenetic Regulators of Redox Homeostasis: A Systematic Review and Meta-Analysis.","authors":"Cristina Mas-Bargues, Javier Huete-Acevedo, Marta Arnal-Forné, Laura Sireno, Virgilio Pérez, Consuelo Borrás","doi":"10.3390/antiox14050532","DOIUrl":"10.3390/antiox14050532","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are emerging as key regulators of cellular communication, with increasing evidence supporting their role in oxidative stress (OS) modulation. In particular, the miRNA cargo of EVs plays a crucial role in mitigating OS and promoting redox balance through both direct antioxidant effects and epigenetic regulation. This study aimed to evaluate the impact of EVs on OS markers, influenced by their miRNA-mediated effects and potential epigenetic modifications in target cells. A systematic literature search was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines to identify studies reporting the effects of EVs on OS parameters. A meta-analysis was performed on key OS biomarkers, including reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA). The heterogeneity of EV isolation and characterization techniques was also analyzed. The included studies demonstrated that EVs exert significant antioxidant effects by reducing ROS levels, increasing SOD activity and GSH levels, and lowering MDA levels. These effects were largely attributed to EV-miRNAs, which induce epigenetic modifications that modulate redox-related signaling pathways. However, the variability in EV isolation methods and characterization approaches highlights the need for standardization to improve data comparability. Despite their therapeutic potential, this significant heterogeneity in EV research remains a barrier to translation. Moreover, further exploration of epigenetic mechanisms is essential to fully harness their benefits for OS-related diseases.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155703","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":"Encapsulation of Polyphenolic Preparation in Gelatin Fruit Jellies Slows the Digestive Release of Cholinesterase Inhibitors In Vitro.","authors":"Dominik Szwajgier, Ewa Baranowska-Wójcik, Wirginia Kukula-Koch, Katarzyna Krzos","doi":"10.3390/antiox14050535","DOIUrl":"10.3390/antiox14050535","url":null,"abstract":"<p><p>Peach, apricot, chokeberry, blueberry, cranberry, raspberry, and wild strawberry fruits were used to create a polyphenolic preparation (PP) after enzyme-assisted extraction, ultrafiltration, and concentration. The composition of PP was determined using LC-MS. Gelatin jellies produced with PP, as well as liquid PP, were \"digested\" in an in vitro model. The entrapment of PP in the gelatin matrix delayed the release of total polyphenolics, flavonoids, flavanols, condensed tannins, and anthocyanins (predominantly during the \"small intestinal\" phase). PP entrapped in the jelly more effectively (<i>p</i> < 0.05) decreased the activity of acetylcholinesterase, butyrylcholinesterase, cyclooxygenase-2 and catalase (during the \"small intestinal\" phase). However, no significant (<i>p</i> < 0.05) effects on superoxide dismutase, glutathione peroxidase, and glutathione reductase activities were observed. FRAP, CUPRAC, HORAC, oxidation of linoleic acid, and ABTS-reducing activities were higher during the \"intestinal\" phase; however, the DPPH test and β-carotene bleaching tests did not confirm these results. The presented findings may be useful for designing nutraceuticals with programmed release of bioactive compounds during digestion.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155801","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":"Regenerative Organic Agriculture and Human Health: The Interconnection Between Soil, Food Quality, and Nutrition.","authors":"Giulia Feliziani, Laura Bordoni, Rosita Gabbianelli","doi":"10.3390/antiox14050530","DOIUrl":"10.3390/antiox14050530","url":null,"abstract":"<p><p>Regenerative organic agriculture (ROA) combines ecological and organic principles to promote soil health, biodiversity, and long-term sustainability. This narrative review explores the connection between soil quality, food nutritional value, and human health, highlighting how ROA can enhance phytochemical content and reduce harmful residues in plant-based foods. Empirical studies report increases in vitamin C, zinc, and polyphenols in crops such as leafy greens, grapes, and carrots grown under regenerative systems, along with reductions in nitrates and pesticide residues. We summarize recent literature (2000-2025) that links soil-driven improvements in food composition to antioxidant activity and potential health benefits. By addressing current research gaps, this review supports the role of ROA in building resilient food systems and preventing chronic disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155858","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":"The Role of Oxidative Stress-Induced Senescence in the Pathogenesis of Preeclampsia.","authors":"Alexandra Barbouti, Dimitrios N Varvarousis, Panagiotis Kanavaros","doi":"10.3390/antiox14050529","DOIUrl":"10.3390/antiox14050529","url":null,"abstract":"<p><p>Preeclampsia is a hypertension condition of human pregnancy that poses a significant risk to pregnant women and their fetus. It complicates about 2-8% of human pregnancies worldwide and displays multifactorial pathogenesis, including increased placental oxidative stress because of disturbed utero-placental blood flow. Recent evidence suggests that increased oxidative stress promotes acceleration of the placental senescence which is implicated in the pathogenesis of preeclampsia. This review focuses on the mechanisms that lead to oxidative stress in preeclamptic patients and examines the role of oxidative stress-induced placental senescence in the pathogenesis of the disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155809","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":"Ferroptosis and Iron Homeostasis: Molecular Mechanisms and Neurodegenerative Disease Implications.","authors":"Nurzhan Abdukarimov, Kamilya Kokabi, Jeannette Kunz","doi":"10.3390/antiox14050527","DOIUrl":"10.3390/antiox14050527","url":null,"abstract":"<p><p>Iron dysregulation has emerged as a pivotal factor in neurodegenerative pathologies, especially through its capacity to promote ferroptosis, a unique form of regulated cell death driven by iron-catalyzed lipid peroxidation. This review synthesizes current evidence on the molecular underpinnings of ferroptosis, focusing on how disruptions in iron homeostasis interact with key antioxidant defenses, such as the system Xc^--glutathione-GPX4 axis, to tip neurons toward lethal oxidative damage. Building on these mechanistic foundations, we explore how ferroptosis intersects with hallmark pathologies in Alzheimer's disease (AD) and Parkinson's disease (PD) and examine how iron accumulation in vulnerable brain regions may fuel disease-specific protein aggregation and neurodegeneration. We further surveyed the distinct components of ferroptosis, highlighting the role of lipid peroxidation enzymes, mitochondrial dysfunction, and recently discovered parallel pathways that either exacerbate or mitigate neuronal death. Finally, we discuss how these insights open new avenues for neuroprotective strategies, including iron chelation and lipid peroxidation inhibitors. By highlighting open questions, this review seeks to clarify the current state of knowledge and proposes directions to harness ferroptosis modulation for disease intervention.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155616","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":"Zearalenone Exposure Damages Skeletal Muscle Through Oxidative Stress and Is Alleviated by Glutathione, Nicotinamide Mononucleotide, and Melatonin.","authors":"Dandan Li, Wei Fu, Jiyue Zhang, Yaqiu Lin, Xianrong Xiong, Jian Li, Yan Xiong","doi":"10.3390/antiox14050528","DOIUrl":"10.3390/antiox14050528","url":null,"abstract":"<p><p>Zearalenone (ZEN), a mycotoxin, is toxic to skeletal muscle, and the solution to alleviate its damage remains unknown. Here, we analyzed the toxic effect of ZEN on muscle and the mitigation of antioxidants (GSH, NMN, and melatonin) for this toxicity. The results showed that 0.02 mmol/L ZEN inhibited myoblast viability and myogenic differentiation, accompanied by reducing <i>Type I</i> and <i>Type IIA</i> and increasing <i>Type IIX</i> myofibers. Antioxidants (NMN with 0.5 mmol/L, GSH with 1 mmol/L, and melatonin with 1 mmol/L) rescued these phenotypes. Mice that were delivered 3 mg/kg body weight (BW)/day of ZEN by gavage for 35 days exhibited a similar trend of muscle fiber composition, but the gavage of antioxidants (NMN with 500 mg/kg BW/day, GSH with 300 mg/kg BW/day, and melatonin with 100 mg/kg BW/day) abolished this phenotype. Mechanistically, ZEN treatment increased ROS production, resulting in oxidative stress, mitochondrial dysfunction, and, subsequently, myofiber changes. Additionally, ZEN indirectly contributed to its damage, decreasing the abundance of <i>Lactobacillus</i> at the genus level and increasing <i>Streptococcus</i> sp. at the species level, which was associated with lactic acid production. Antioxidants partially rescued this microbiota composition. This study explores ZEN toxicity effects and alleviation of antioxidants, which provides new insights and attenuation solutions for ZEN damage to skeletal muscle. However, the underlying molecular mechanism of ZEN and antioxidants in the skeletal muscle still needs to be explored.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12108299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155816","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}