Ammonia is a key water quality factor limiting shrimp aquaculture. Intestinal health is closely associated with the nutrition, metabolism and immunity of shrimp. However, the response characteristics of the shrimp intestine to ammonia stress under seawater and low-salinity environments remain unclear. In this study, the shrimp Litopenaeus vannamei reared in seawater (salinity 30) or low-salinity (salinity 3) water were subjected to ammonia stress for 14 days, respectively. The changes in intestinal morphology, antioxidant capacity, immune response, energy metabolism, and microbial community were systematically investigated. The results showed that ammonia stress induced intestinal tissue damage in both seawater and low-salinity cultured shrimp, characterized by epithelial cell detachment and mucosal structural disruption. At the molecular level, ammonia stress triggered intestinal stress responses by interfering with key physiological processes such as antioxidant defense and endoplasmic reticulum stress. This process further led to varying degrees of disorders in physiological functions, including immune regulation, inflammatory response, and autophagic activity. In addition, ammonia stress disrupted the homeostatic balance of intestinal energy metabolism by affecting the expression of genes related to glucose metabolism, the tricarboxylic acid (TCA) cycle, and mitochondrial respiratory chain. In addition, ammonia stress increased the diversity of intestinal microbiota and caused microbial dysbiosis by increasing harmful bacteria (e.g., Vibrio) and decreasing beneficial bacterial groups (e.g., Bacillus). Ammonia stress generally enhanced intestinal microbiota chemotaxis. Specifically, predicted functions of microbiota in seawater-cultured shrimp showed increased carbohydrate, linoleic acid, and cofactor/vitamin metabolism; in low-salinity-cultured shrimp, functions including protein digestion/absorption, flavonoid/steroid hormone biosynthesis, and glycosaminoglycan degradation were reduced. These results revealed that ammonia stress compromised shrimp intestinal health by disrupting mucosal structure, triggering stress responses, and disturbing immune function, energy metabolism, and microbial homeostasis. Notably, low-salinity cultured shrimp exhibited more pronounced intestinal stress responses and greater physiological vulnerability than seawater-cultured counterparts.
{"title":"Ammonia Stress Disrupts Intestinal Health in <i>Litopenaeus vannamei</i> Under Seawater and Low-Salinity Environments by Impairing Mucosal Integrity, Antioxidant Capability, Immunity, Energy Metabolism, and Microbial Community.","authors":"Yafei Duan, Yuxiu Nan, Jitao Li, Meng Xiao, Yun Wang, Ruijie Zhu","doi":"10.3390/antiox14111383","DOIUrl":"https://doi.org/10.3390/antiox14111383","url":null,"abstract":"<p><p>Ammonia is a key water quality factor limiting shrimp aquaculture. Intestinal health is closely associated with the nutrition, metabolism and immunity of shrimp. However, the response characteristics of the shrimp intestine to ammonia stress under seawater and low-salinity environments remain unclear. In this study, the shrimp <i>Litopenaeus vannamei</i> reared in seawater (salinity 30) or low-salinity (salinity 3) water were subjected to ammonia stress for 14 days, respectively. The changes in intestinal morphology, antioxidant capacity, immune response, energy metabolism, and microbial community were systematically investigated. The results showed that ammonia stress induced intestinal tissue damage in both seawater and low-salinity cultured shrimp, characterized by epithelial cell detachment and mucosal structural disruption. At the molecular level, ammonia stress triggered intestinal stress responses by interfering with key physiological processes such as antioxidant defense and endoplasmic reticulum stress. This process further led to varying degrees of disorders in physiological functions, including immune regulation, inflammatory response, and autophagic activity. In addition, ammonia stress disrupted the homeostatic balance of intestinal energy metabolism by affecting the expression of genes related to glucose metabolism, the tricarboxylic acid (TCA) cycle, and mitochondrial respiratory chain. In addition, ammonia stress increased the diversity of intestinal microbiota and caused microbial dysbiosis by increasing harmful bacteria (e.g., <i>Vibrio</i>) and decreasing beneficial bacterial groups (e.g., <i>Bacillus</i>). Ammonia stress generally enhanced intestinal microbiota chemotaxis. Specifically, predicted functions of microbiota in seawater-cultured shrimp showed increased carbohydrate, linoleic acid, and cofactor/vitamin metabolism; in low-salinity-cultured shrimp, functions including protein digestion/absorption, flavonoid/steroid hormone biosynthesis, and glycosaminoglycan degradation were reduced. These results revealed that ammonia stress compromised shrimp intestinal health by disrupting mucosal structure, triggering stress responses, and disturbing immune function, energy metabolism, and microbial homeostasis. Notably, low-salinity cultured shrimp exhibited more pronounced intestinal stress responses and greater physiological vulnerability than seawater-cultured counterparts.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627703","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}
Meral Karakoç, Hayat Ayaz, Ferhat Çelik, Fırat Aşır
Background: Peripheral nerve injuries frequently result in incomplete recovery despite advances in microsurgical repair. Both pharmacological and rehabilitative strategies have been investigated to enhance regeneration. Dexamethasone, a potent anti-inflammatory corticosteroid, and aerobic exercise, such as swimming, may promote repair through distinct but complementary mechanisms.
Methods: A standardized rat sciatic nerve crush model was used to evaluate the effects of local dexamethasone administration (2 mg/kg/day, perineural for 10 days), swimming exercise (20 min/session, three times per week for 21 days), and their combination. Functional recovery was assessed by the Sciatic Functional Index (SFI), oxidative stress by MDA, GPX, and MPO assays, and structural recovery by histological, MBP immunohistochemical, and TEM analyses.
Results: The injury group exhibited markedly elevated MDA and MPO levels and reduced GPX activity, indicating oxidative stress. Both dexamethasone and swimming exercise significantly improved these parameters, while the combination group showed values approaching controls (p < 0.001 for all comparisons vs. injury). Histological and immunohistochemical findings confirmed greater myelin preservation and higher MBP expression in treated groups, particularly in the combination group, whose g-ratio and myelin thickness were statistically indistinguishable from controls. SFI analysis revealed progressive motor improvement, with the combination therapy achieving near-normal function by day 28.
Conclusions: This study demonstrates that dexamethasone and swimming exercise each contribute to peripheral nerve recovery and that their combined application provides additive benefits in terms of functional, biochemical, and structural regeneration. These results are limited to the specific dose and exercise regimen tested but support the potential of integrating anti-inflammatory pharmacotherapy with controlled physical exercise as a multimodal approach to enhance peripheral nerve repair.
{"title":"Evaluation of Dexamethasone and Swimming Exercise as Complementary Interventions in a Rat Sciatic Nerve Injury Model.","authors":"Meral Karakoç, Hayat Ayaz, Ferhat Çelik, Fırat Aşır","doi":"10.3390/antiox14111382","DOIUrl":"https://doi.org/10.3390/antiox14111382","url":null,"abstract":"<p><strong>Background: </strong>Peripheral nerve injuries frequently result in incomplete recovery despite advances in microsurgical repair. Both pharmacological and rehabilitative strategies have been investigated to enhance regeneration. Dexamethasone, a potent anti-inflammatory corticosteroid, and aerobic exercise, such as swimming, may promote repair through distinct but complementary mechanisms.</p><p><strong>Methods: </strong>A standardized rat sciatic nerve crush model was used to evaluate the effects of local dexamethasone administration (2 mg/kg/day, perineural for 10 days), swimming exercise (20 min/session, three times per week for 21 days), and their combination. Functional recovery was assessed by the Sciatic Functional Index (SFI), oxidative stress by MDA, GPX, and MPO assays, and structural recovery by histological, MBP immunohistochemical, and TEM analyses.</p><p><strong>Results: </strong>The injury group exhibited markedly elevated MDA and MPO levels and reduced GPX activity, indicating oxidative stress. Both dexamethasone and swimming exercise significantly improved these parameters, while the combination group showed values approaching controls (<i>p</i> < 0.001 for all comparisons vs. injury). Histological and immunohistochemical findings confirmed greater myelin preservation and higher MBP expression in treated groups, particularly in the combination group, whose g-ratio and myelin thickness were statistically indistinguishable from controls. SFI analysis revealed progressive motor improvement, with the combination therapy achieving near-normal function by day 28.</p><p><strong>Conclusions: </strong>This study demonstrates that dexamethasone and swimming exercise each contribute to peripheral nerve recovery and that their combined application provides additive benefits in terms of functional, biochemical, and structural regeneration. These results are limited to the specific dose and exercise regimen tested but support the potential of integrating anti-inflammatory pharmacotherapy with controlled physical exercise as a multimodal approach to enhance peripheral nerve repair.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627929","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}
Ji Chen, Chunyan Ma, Xu Mo, Linhong Li, Lijuan Wu, Chaowen Zhang, Rui Li, Yuanfeng Zou, Fan Liu, Mengliang Tian
Dendrobium moschatum neutral polysaccharide (DMP-NP) was isolated using a water extraction-ethanol precipitation method, followed by purification with DEAE-cellulose anion-exchange resin and a dextran gel column. The resulting DMP-NP1 exhibited a weight-average molecular weight of 16.23 kDa. The molar ratio of monosaccharides was as follows: glucose-mannose-galactose-fucose-rhamnose = 78.54:19.11:1.59:0.53:0.23, with a glucose-to-mannose ratio of 4.1:1. Infrared spectroscopic analysis revealed characteristic carbohydrate absorption peaks and confirmed the presence of pyranosidic linkages. NMR analysis revealed that DMP-NP1 possesses a backbone mainly formed by 1→4 glycosidic linkages, a small number of 1→6 branches, and O-acetyl substitutions at the C2 and C3 positions of mannose residues. In vitro experiments demonstrated that treatment with 0-20 μg/mL (0-1.23 μM) DMP-NP significantly enhanced the activities of catalase (CAT) and superoxide dismutase (SOD) in IPEC-J2 cells, along with upregulation of the corresponding antioxidant genes. Concurrently, DMP-NP reduced the secretion of key pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, and downregulated the expression of genes associated with both antioxidant and inflammatory signaling pathways. Collectively, these findings indicate that DMP-NP not only prevents but also ameliorates LPS-induced inflammatory injury in intestinal epithelial cells, thereby providing a basis for the application of DMP-NP in intestinal inflammation mitigation.
{"title":"Anti-Inflammatory and Antioxidant Mechanisms of <i>Dendrobium moschatum</i> Polysaccharide in Intestinal Epithelial Cells via TLR4-NF-κB and Nrf2 Signaling Pathways.","authors":"Ji Chen, Chunyan Ma, Xu Mo, Linhong Li, Lijuan Wu, Chaowen Zhang, Rui Li, Yuanfeng Zou, Fan Liu, Mengliang Tian","doi":"10.3390/antiox14111384","DOIUrl":"https://doi.org/10.3390/antiox14111384","url":null,"abstract":"<p><p><i>Dendrobium moschatum</i> neutral polysaccharide (DMP-NP) was isolated using a water extraction-ethanol precipitation method, followed by purification with DEAE-cellulose anion-exchange resin and a dextran gel column. The resulting DMP-NP1 exhibited a weight-average molecular weight of 16.23 kDa. The molar ratio of monosaccharides was as follows: glucose-mannose-galactose-fucose-rhamnose = 78.54:19.11:1.59:0.53:0.23, with a glucose-to-mannose ratio of 4.1:1. Infrared spectroscopic analysis revealed characteristic carbohydrate absorption peaks and confirmed the presence of pyranosidic linkages. NMR analysis revealed that DMP-NP1 possesses a backbone mainly formed by 1→4 glycosidic linkages, a small number of 1→6 branches, and O-acetyl substitutions at the C2 and C3 positions of mannose residues. In vitro experiments demonstrated that treatment with 0-20 μg/mL (0-1.23 μM) DMP-NP significantly enhanced the activities of catalase (CAT) and superoxide dismutase (SOD) in IPEC-J2 cells, along with upregulation of the corresponding antioxidant genes. Concurrently, DMP-NP reduced the secretion of key pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, and downregulated the expression of genes associated with both antioxidant and inflammatory signaling pathways. Collectively, these findings indicate that DMP-NP not only prevents but also ameliorates LPS-induced inflammatory injury in intestinal epithelial cells, thereby providing a basis for the application of DMP-NP in intestinal inflammation mitigation.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627738","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}
Diana Barros, Liliana Grenho, Maria Helena Fernandes, Pedro Sousa Gomes, Élia Fernandes
This study explores the antioxidant, antibacterial, and cytocompatibility properties of aqueous Pinus pinaster bark extract (PBE). PBE was prepared using two solvent systems-100% distilled water and 1% DMSO in aqueous solution-at a solid-to-liquid ratio of 1:20 (w/v), following ISO guidelines. Extract characterization included yield determination, FTIR analysis, quantification of total phenolic (TPC) and flavonoid (TFC) contents, and assessment of antioxidant activity using four complementary methods: free radical scavenging (DPPH and ABTS), metal ion reduction (FRAP), and a competitive reaction assay (ORAC). The phenolic compound profile was further examined by HPLC-DAD. The results indicated that the two extracts exhibited comparable values across all evaluated parameters when expressed per gram of PBE. The TPC and TFC were approximately 400 mg GAE (gallic acid equivalents)/g PBE and 92 mg CE (catechin equivalents)/g PBE, respectively. Antioxidant capacity values were about 880, 1030, 3210, and 585 mg TE (Trolox equivalents)/g PBE for the DPPH, ABTS, ORAC, and FRAP assays, respectively. Furthermore, in both extracts, the phenolic and flavonoid contents exhibited strong positive correlations with antioxidant activity across all four chemical assays. The 100% aqueous extract was additionally evaluated for antibacterial activity and cytocompatibility with eukaryotic cells. Compared to the control, the extract demonstrated IC50 values of 0.304, 0.678, and 0.845 mg/mL PBE for the inhibition of Staphylococcus aureus, Escherichia coli, and fibroblast cells, respectively. Antioxidant and antibacterial activities showed a positive association within concentration ranges that remained non-cytotoxic to fibroblasts. Overall, these findings indicate that the aqueous PBE retains cytocompatibility across a wide concentration range while maintaining both antioxidant and antibacterial activities, underscoring its potential for biological applications involving direct contact with eukaryotic cells.
{"title":"Correlation of Antioxidant and Antibacterial Activities of the Aqueous <i>Pinus pinaster</i> Aiton Bark Extract Within a Cytocompatible Concentration Range.","authors":"Diana Barros, Liliana Grenho, Maria Helena Fernandes, Pedro Sousa Gomes, Élia Fernandes","doi":"10.3390/antiox14111377","DOIUrl":"https://doi.org/10.3390/antiox14111377","url":null,"abstract":"<p><p>This study explores the antioxidant, antibacterial, and cytocompatibility properties of aqueous <i>Pinus pinaster</i> bark extract (PBE). PBE was prepared using two solvent systems-100% distilled water and 1% DMSO in aqueous solution-at a solid-to-liquid ratio of 1:20 (<i>w</i>/<i>v</i>), following ISO guidelines. Extract characterization included yield determination, FTIR analysis, quantification of total phenolic (TPC) and flavonoid (TFC) contents, and assessment of antioxidant activity using four complementary methods: free radical scavenging (DPPH and ABTS), metal ion reduction (FRAP), and a competitive reaction assay (ORAC). The phenolic compound profile was further examined by HPLC-DAD. The results indicated that the two extracts exhibited comparable values across all evaluated parameters when expressed per gram of PBE. The TPC and TFC were approximately 400 mg GAE (gallic acid equivalents)/g PBE and 92 mg CE (catechin equivalents)/g PBE, respectively. Antioxidant capacity values were about 880, 1030, 3210, and 585 mg TE (Trolox equivalents)/g PBE for the DPPH, ABTS, ORAC, and FRAP assays, respectively. Furthermore, in both extracts, the phenolic and flavonoid contents exhibited strong positive correlations with antioxidant activity across all four chemical assays. The 100% aqueous extract was additionally evaluated for antibacterial activity and cytocompatibility with eukaryotic cells. Compared to the control, the extract demonstrated IC<sub>50</sub> values of 0.304, 0.678, and 0.845 mg/mL PBE for the inhibition of <i>Staphylococcus aureus</i>, <i>Escherichia coli</i>, and fibroblast cells, respectively. Antioxidant and antibacterial activities showed a positive association within concentration ranges that remained non-cytotoxic to fibroblasts. Overall, these findings indicate that the aqueous PBE retains cytocompatibility across a wide concentration range while maintaining both antioxidant and antibacterial activities, underscoring its potential for biological applications involving direct contact with eukaryotic cells.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627950","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}
Maja Ledinski, Katarina Caput Mihalić, Marijana Šimić Jovičić, Karla Ostojić, Zara Škibola, Robert Kolundžić, Inga Urlić
The resilience of sarcomas, tumors characterized by resistance to therapy and high metastatic potential, is largely driven by the unique characteristics of a small population known as cancer stem cells (CSC). Although ascorbic acid (AA) and its oxidized form, dehydroascorbic acid (DHA), have shown potential for selectively targeting cancer cells, their effects on sarcoma CSCs remain insufficiently explored. Still, recent research indicates that AA can affect the specific characteristics of CSC and lead to their cytotoxicity. To investigate the sensitivity of sarcoma CSCs to ascorbate, CSCs were isolated from six sarcoma patient-derived samples using a sphere assay, and their stem identity was evaluated through gene expression profiling and dye-efflux assays. Cytotoxicity testing of AA and DHA showed that DHA has a selective cytotoxic effect on cancer stem cells. The presence of basic fibroblast growth factor (bFGF), which is commonly used to support the self-renewal of CSCs, had an influence on the cytotoxic effect of DHA. To evaluate the difference in the effect of AA and DHA, a seven-day treatment of CSCs with these forms of ascorbate was performed. The gene expression analysis revealed that DHA in the presence of bFGF had a stronger impact on response to oxidative stress and cellular metabolism. Also, investigation of somatic mutations of oncogenes and tumor suppressors revealed that in liposarcoma and rhabdomyosarcoma, there are mutations that induce proliferative signals. These proliferative signals, joined with bFGF in the presence of DHA, do not lead to proliferation but instead cause cell death.
{"title":"Dehydroascorbic Acid Induces Cell Death in Sarcoma Stem Cells Under bFGF-Mediated Stemness-Supporting Conditions.","authors":"Maja Ledinski, Katarina Caput Mihalić, Marijana Šimić Jovičić, Karla Ostojić, Zara Škibola, Robert Kolundžić, Inga Urlić","doi":"10.3390/antiox14111376","DOIUrl":"https://doi.org/10.3390/antiox14111376","url":null,"abstract":"<p><p>The resilience of sarcomas, tumors characterized by resistance to therapy and high metastatic potential, is largely driven by the unique characteristics of a small population known as cancer stem cells (CSC). Although ascorbic acid (AA) and its oxidized form, dehydroascorbic acid (DHA), have shown potential for selectively targeting cancer cells, their effects on sarcoma CSCs remain insufficiently explored. Still, recent research indicates that AA can affect the specific characteristics of CSC and lead to their cytotoxicity. To investigate the sensitivity of sarcoma CSCs to ascorbate, CSCs were isolated from six sarcoma patient-derived samples using a sphere assay, and their stem identity was evaluated through gene expression profiling and dye-efflux assays. Cytotoxicity testing of AA and DHA showed that DHA has a selective cytotoxic effect on cancer stem cells. The presence of basic fibroblast growth factor (bFGF), which is commonly used to support the self-renewal of CSCs, had an influence on the cytotoxic effect of DHA. To evaluate the difference in the effect of AA and DHA, a seven-day treatment of CSCs with these forms of ascorbate was performed. The gene expression analysis revealed that DHA in the presence of bFGF had a stronger impact on response to oxidative stress and cellular metabolism. Also, investigation of somatic mutations of oncogenes and tumor suppressors revealed that in liposarcoma and rhabdomyosarcoma, there are mutations that induce proliferative signals. These proliferative signals, joined with bFGF in the presence of DHA, do not lead to proliferation but instead cause cell death.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627935","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}
Jelly is a popular confectionery, and research increasingly focuses on nutritionally enhanced formulations. In this study, gelatin capsule waste was valorized as a natural gelling base for chamomile jelly, providing an innovative approach to upcycling food-grade waste into functional products. The effects of replacing sugar with inulin (INU) or polydextrose (PDX) (25-100%) on chemical, physical, and sensory properties were investigated. Sugar replacement decreased carbohydrate content while increasing ash and fat, slightly increased turbidity, and reduced lightness (L*) and yellowness (b*). Gels with inulin and polydextrose exhibited higher gel strength (55.97-81.45 g) and hardness (9.77-10.20 N) than the control, whereas antioxidant activity remained largely unaffected. Among the formulations, 50% inulin (INU-50) received the highest consumer acceptance score (6.88 ± 1.05) and maintained stable quality during 21 days at 4 °C, with decreased free water content and increased gel strength. INU-50 jelly supplied essential nutrients, was cholesterol-free, and promoted Lactobacillus plantarum growth, supported by metabolomic analysis. Overall, this study demonstrates the potential of chamomile jelly with inulin substitution as a functional, health-promoting product and highlights a novel, sustainable approach to valorize gelatin capsule waste for modern health-conscious consumers.
{"title":"Functional and Metabolomic Analyses of Chamomile Jelly Derived from Gelatin Capsule Waste with Inulin and Polydextrose as Prebiotic Sugar Substitutes.","authors":"Sasina Sanprasert, Anurak Uchuwittayakul, Pudthaya Kumnerdsiri, Lalitphan Kitsanayanyong, Anusorn Seubsai, Jaksuma Pongsetkul, Kantiya Petsong, Supatra Karnjanapratum, Chalalai Jaisan, Samart Sai-Ut, Saroat Rawdkuen, Passakorn Kingwascharapong","doi":"10.3390/antiox14111380","DOIUrl":"https://doi.org/10.3390/antiox14111380","url":null,"abstract":"<p><p>Jelly is a popular confectionery, and research increasingly focuses on nutritionally enhanced formulations. In this study, gelatin capsule waste was valorized as a natural gelling base for chamomile jelly, providing an innovative approach to upcycling food-grade waste into functional products. The effects of replacing sugar with inulin (INU) or polydextrose (PDX) (25-100%) on chemical, physical, and sensory properties were investigated. Sugar replacement decreased carbohydrate content while increasing ash and fat, slightly increased turbidity, and reduced lightness (<i>L*</i>) and yellowness (<i>b*</i>). Gels with inulin and polydextrose exhibited higher gel strength (55.97-81.45 g) and hardness (9.77-10.20 N) than the control, whereas antioxidant activity remained largely unaffected. Among the formulations, 50% inulin (INU-50) received the highest consumer acceptance score (6.88 ± 1.05) and maintained stable quality during 21 days at 4 °C, with decreased free water content and increased gel strength. INU-50 jelly supplied essential nutrients, was cholesterol-free, and promoted <i>Lactobacillus plantarum</i> growth, supported by metabolomic analysis. Overall, this study demonstrates the potential of chamomile jelly with inulin substitution as a functional, health-promoting product and highlights a novel, sustainable approach to valorize gelatin capsule waste for modern health-conscious consumers.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627965","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}
Yugyeong Sim, Jin-Hyoung Kim, Jeong-Soo Lee, Jinyoung Jeong, Hyun-Ju Cho
Nanoplastics have been recognized as emerging pollutants posing potential risks to ecosystems and human health. They are now detected ubiquitously in the environment and even human tissues, where their small size allows for tissue accumulation and cellular penetration. Growing evidence links nanoplastics to oxidative stress, yet the specific contribution of extracellular accumulation to toxicity remains poorly understood. To address this, we used zebrafish, a transparent vertebrate model suitable for toxicological studies, to explore the role of extracellular antioxidant defenses in polystyrene nanoplastic (PSNP)-induced oxidative stress. In particular, we focused on superoxide dismutase 3 (SOD3), which is an enzyme that regulates extracellular reactive oxygen species by catalyzing the detoxification of superoxide radicals. Zebrafish Sod3a is a homolog of human SOD3, preserving conserved metal-binding sites critical for enzymatic function. We established sod3a mutant zebrafish and examined their responses following PSNP exposure. In sod3a mutant larvae, tissue accumulation of PSNPs was higher than in wild-type (WT), and this was associated with elevated oxidative stress, enhanced cell death, and abnormalities in intestinal function and immune responses. Collectively, these observations reveal the functional importance of SOD3 during PSNP-induced oxidative stress and provide new insight into extracellular antioxidant mechanisms that mitigate PSNP-induced toxicity.
{"title":"Superoxide Dismutase 3 Deficiency Disrupts the Regulation of Oxidative Stress Caused by Polystyrene Nanoplastics.","authors":"Yugyeong Sim, Jin-Hyoung Kim, Jeong-Soo Lee, Jinyoung Jeong, Hyun-Ju Cho","doi":"10.3390/antiox14111378","DOIUrl":"https://doi.org/10.3390/antiox14111378","url":null,"abstract":"<p><p>Nanoplastics have been recognized as emerging pollutants posing potential risks to ecosystems and human health. They are now detected ubiquitously in the environment and even human tissues, where their small size allows for tissue accumulation and cellular penetration. Growing evidence links nanoplastics to oxidative stress, yet the specific contribution of extracellular accumulation to toxicity remains poorly understood. To address this, we used zebrafish, a transparent vertebrate model suitable for toxicological studies, to explore the role of extracellular antioxidant defenses in polystyrene nanoplastic (PSNP)-induced oxidative stress. In particular, we focused on superoxide dismutase 3 (SOD3), which is an enzyme that regulates extracellular reactive oxygen species by catalyzing the detoxification of superoxide radicals. Zebrafish Sod3a is a homolog of human SOD3, preserving conserved metal-binding sites critical for enzymatic function. We established <i>sod3a</i> mutant zebrafish and examined their responses following PSNP exposure. In <i>sod3a</i> mutant larvae, tissue accumulation of PSNPs was higher than in wild-type (WT), and this was associated with elevated oxidative stress, enhanced cell death, and abnormalities in intestinal function and immune responses. Collectively, these observations reveal the functional importance of SOD3 during PSNP-induced oxidative stress and provide new insight into extracellular antioxidant mechanisms that mitigate PSNP-induced toxicity.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627493","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}
Maria Luisa Valle, Bitseat Getaneh, Christopher William, Jorge Ghiso, Agueda Rostagno
Cerebral amyloid angiopathy (CAA), present in more than 90% of Alzheimer's disease (AD) cases, associates with focal ischemia and neurovascular dysfunction. Genetic variants at positions 21-23 of amyloid beta (Aβ), among them the Dutch mutation (AβE22Q), are primarily linked to CAA and the development of cerebral hemorrhages. An important contributor to CAA pathogenesis is the dysregulation of mitochondria-mediated pathways with concomitant induction of oxidative stress. Using biochemical assays and immunofluorescence microscopy, this work demonstrates the exacerbated formation of reactive oxygen species (ROS) in human brain microvascular endothelial cells after short exposure to soluble oligomers of synthetic homologues of Aβ1-42 and the Dutch variant, inducing lipid peroxidation and protein carbonylation, both markers of oxidative stress. The heterogeneity of the soluble oligomeric assemblies inducing this oxidative response was highlighted by their reactivity with two conformational antibodies recognizing specific and mutually exclusive epitopes associated with either soluble prefibrillar oligomers or soluble fibrillar oligomers. Treatment with the multitarget antioxidants Trolox and methazolamide significantly attenuated the Aβ-mediated ROS production and reduced oxidative stress markers to basal levels. Our data highlight the damaging role of heterogeneous Aβ oligomers and the preventing effect of antioxidants, suggesting ROS modulation as a complementary therapeutic strategy to preserve neurovascular unit integrity.
{"title":"Antioxidants Trolox and Methazolamide Protect Microvascular Endothelial Cells from Oxidative Damage Induced by Sporadic and Familial Forms of Oligomeric Amyloid-β.","authors":"Maria Luisa Valle, Bitseat Getaneh, Christopher William, Jorge Ghiso, Agueda Rostagno","doi":"10.3390/antiox14111375","DOIUrl":"https://doi.org/10.3390/antiox14111375","url":null,"abstract":"<p><p>Cerebral amyloid angiopathy (CAA), present in more than 90% of Alzheimer's disease (AD) cases, associates with focal ischemia and neurovascular dysfunction. Genetic variants at positions 21-23 of amyloid beta (Aβ), among them the Dutch mutation (AβE22Q), are primarily linked to CAA and the development of cerebral hemorrhages. An important contributor to CAA pathogenesis is the dysregulation of mitochondria-mediated pathways with concomitant induction of oxidative stress. Using biochemical assays and immunofluorescence microscopy, this work demonstrates the exacerbated formation of reactive oxygen species (ROS) in human brain microvascular endothelial cells after short exposure to soluble oligomers of synthetic homologues of Aβ1-42 and the Dutch variant, inducing lipid peroxidation and protein carbonylation, both markers of oxidative stress. The heterogeneity of the soluble oligomeric assemblies inducing this oxidative response was highlighted by their reactivity with two conformational antibodies recognizing specific and mutually exclusive epitopes associated with either soluble prefibrillar oligomers or soluble fibrillar oligomers. Treatment with the multitarget antioxidants Trolox and methazolamide significantly attenuated the Aβ-mediated ROS production and reduced oxidative stress markers to basal levels. Our data highlight the damaging role of heterogeneous Aβ oligomers and the preventing effect of antioxidants, suggesting ROS modulation as a complementary therapeutic strategy to preserve neurovascular unit integrity.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627879","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}
Pasquale Crupi, Maria Lisa Clodoveo, Addolorata Desantis, Roberta Zupo, Filomena Corbo
Kinetic evolution of quality parameters in 21 extra-virgin olive oils (EVOOs) from Coratina cultivar was evaluated during 18 months of dark storage at room temperature (RT) and 4 °C (LT). The aim was to identify the most discriminating variables-fatty acids, peroxide value, spectrophotometric indices, and phenolic compounds-using kinetic analysis and multivariate statistics. Fatty acids remained stable, while peroxide value and ultraviolet absorbance indices increased significantly at RT, following zero-order kinetics. Polyphenols declined markedly after 6 months, especially at RT, with degradation rates influenced by initial concentrations. Hydroxytyrosol and tyrosol followed pseudo-zero-order kinetics, whereas secoiridoids and lignans followed second-order kinetics. Discriminant analysis achieved 90% accuracy (p = 0.000012) in classifying oils by storage condition. The most relevant discriminants were associated with phenolic degradation and oxidative changes. These findings support the importance of low-temperature storage in preserving the biochemical quality and shelf life of EVOOs.
{"title":"Effect of Long-Term Storage Temperature on the Quality of Extra-Virgin Olive Oil (Coratina cv.): A Multivariate Discriminant Approach.","authors":"Pasquale Crupi, Maria Lisa Clodoveo, Addolorata Desantis, Roberta Zupo, Filomena Corbo","doi":"10.3390/antiox14111379","DOIUrl":"https://doi.org/10.3390/antiox14111379","url":null,"abstract":"<p><p>Kinetic evolution of quality parameters in 21 extra-virgin olive oils (EVOOs) from Coratina cultivar was evaluated during 18 months of dark storage at room temperature (RT) and 4 °C (LT). The aim was to identify the most discriminating variables-fatty acids, peroxide value, spectrophotometric indices, and phenolic compounds-using kinetic analysis and multivariate statistics. Fatty acids remained stable, while peroxide value and ultraviolet absorbance indices increased significantly at RT, following zero-order kinetics. Polyphenols declined markedly after 6 months, especially at RT, with degradation rates influenced by initial concentrations. Hydroxytyrosol and tyrosol followed pseudo-zero-order kinetics, whereas secoiridoids and lignans followed second-order kinetics. Discriminant analysis achieved 90% accuracy (<i>p</i> = 0.000012) in classifying oils by storage condition. The most relevant discriminants were associated with phenolic degradation and oxidative changes. These findings support the importance of low-temperature storage in preserving the biochemical quality and shelf life of EVOOs.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627805","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}
Anna Schwantes, Yara Shadid, Vanesa Maria Guerrero Ruiz, Blerina Aliraj, Anja Wickert, Megan A Palmer, Sofie P Meyer, Andreas Weigert, Bernhard Brüne, Dominik C Fuhrmann
Glioblastoma is one of the most aggressive and therapeutically challenging brain tumors. It is characterized by a highly immunosuppressive tumor microenvironment and poor prognosis, requiring novel treatment strategies. Along this line, ferroptosis has been proposed. To study the impact of ferroptosis on glioblastoma cells and immune cell infiltration, we established a spheroid model using LN229 glioblastoma cells and verified ferroptosis by measuring lipid peroxidation and RNA expression of ferroptosis-related genes. We then co-cultured spheroids with human peripheral blood mononuclear cells to follow the infiltration of distinct immune cell subsets by flow cytometry and immunohistochemistry. T lymphocyte infiltration into ferroptotic spheroids compared to control spheroids became apparent with the notion that ferroptotic cells attracted T cells more efficiently compared to apoptotic or necrotic cells. Mechanistically, ferroptotic glioblastoma spheroids released high amounts of ATP, which caused T cell attraction, while ATP deprivation reduced this effect. Ferroptosis appears to be an interesting therapy approach but might need co-treatments to ensure proper T cell activation.
{"title":"Ferroptosis Enhances T Lymphocyte Infiltration into Glioblastoma Spheroids.","authors":"Anna Schwantes, Yara Shadid, Vanesa Maria Guerrero Ruiz, Blerina Aliraj, Anja Wickert, Megan A Palmer, Sofie P Meyer, Andreas Weigert, Bernhard Brüne, Dominik C Fuhrmann","doi":"10.3390/antiox14111373","DOIUrl":"https://doi.org/10.3390/antiox14111373","url":null,"abstract":"<p><p>Glioblastoma is one of the most aggressive and therapeutically challenging brain tumors. It is characterized by a highly immunosuppressive tumor microenvironment and poor prognosis, requiring novel treatment strategies. Along this line, ferroptosis has been proposed. To study the impact of ferroptosis on glioblastoma cells and immune cell infiltration, we established a spheroid model using LN229 glioblastoma cells and verified ferroptosis by measuring lipid peroxidation and RNA expression of ferroptosis-related genes. We then co-cultured spheroids with human peripheral blood mononuclear cells to follow the infiltration of distinct immune cell subsets by flow cytometry and immunohistochemistry. T lymphocyte infiltration into ferroptotic spheroids compared to control spheroids became apparent with the notion that ferroptotic cells attracted T cells more efficiently compared to apoptotic or necrotic cells. Mechanistically, ferroptotic glioblastoma spheroids released high amounts of ATP, which caused T cell attraction, while ATP deprivation reduced this effect. Ferroptosis appears to be an interesting therapy approach but might need co-treatments to ensure proper T cell activation.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 11","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12649233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627972","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}