Pub Date : 2026-06-01Epub Date: 2026-03-07DOI: 10.1016/j.arres.2026.100161
Joan N. Whittier , Sophia C. Heller , Akalanka Ekanayake , Stephenson B. Owusu , Alexei V. Tivanski , Michael S. Petronek
Several tumor types have shown an iron metabolic phenotype characterized by preferential iron accumulation relative to their normal tissue counterparts. However, the fundamental mechanism(s) by which iron can contribute to tumor progression are still unclear. To test the biophysical role of iron in tumor cell motility, this short communication leveraged a ferritin heavy chain overexpression model system to absorb intracellular labile iron. Using this model system, ferritin overexpression mitigates lipid peroxidation and increases cell stiffness to diminish cell motility.
{"title":"Vector-induced ferritin overexpression limits cell motility by controlling cell stiffness in glioblastoma cells","authors":"Joan N. Whittier , Sophia C. Heller , Akalanka Ekanayake , Stephenson B. Owusu , Alexei V. Tivanski , Michael S. Petronek","doi":"10.1016/j.arres.2026.100161","DOIUrl":"10.1016/j.arres.2026.100161","url":null,"abstract":"<div><div>Several tumor types have shown an iron metabolic phenotype characterized by preferential iron accumulation relative to their normal tissue counterparts. However, the fundamental mechanism(s) by which iron can contribute to tumor progression are still unclear. To test the biophysical role of iron in tumor cell motility, this short communication leveraged a ferritin heavy chain overexpression model system to absorb intracellular labile iron. Using this model system, ferritin overexpression mitigates lipid peroxidation and increases cell stiffness to diminish cell motility.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"19 ","pages":"Article 100161"},"PeriodicalIF":2.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147388465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A family of enzymes known as nitric oxide synthases (NOS) produces nitric oxide (NO), a tiny, unstable, and potentially hazardous gas that is highly diffusible across cell membranes. NO and NO metabolites, such as nitrite, nitrate, S-nitrosothiols, nitrosamines, and peroxynitrite, mediate a variety of cytotoxic and genotoxic effects, such as inhibition of mitochondrial respiration, protein and DNA damage that leads to gene mutation, loss of protein function, necrosis, and apoptosis. Through a variety of apoptotic mechanisms, abnormally elevated NO generation by NOS II/iNOS may cause cytotoxicity of cancer cells. Tetrahydrobiopterin (BH4) is required by all NOS isoforms for NO production. Another way mammalian cells can create BH4 is by the "salvage pathway," which uses sepiapterin reductase and dihydrofolate reductase to convert sepiapterin to BH4. Better apoptotic effects on cancer cells may result from boosting BH4 levels by treating cells with sepiapterin, 7-8-dihydropterin, or pterin derivatives, which work in concert to improve NO levels. Another common medication used to treat and prevent hypercholesterolaemia and related cardiovascular disorders is statins, which lower serum cholesterol. They are competitive inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, the enzyme that limits the rate at which cholesterol is produced. Statins also improve cardiovascular and endothelial function by increasing the generation of nitric oxide (NO) by endothelial cells. They also have an impact on a variety of molecules and signaling pathways that govern the synthesis of apoptotic proteins and raise nitric oxide (NO) levels. Therefore, the NO-mediated route may be used to induce apoptosis due to the synergistic potency of statins and pterin derivatives. This review focusses on the effectiveness of statins and pterin derivatives, as well as their ability to influence the production of nitric oxide, which intensifies the effect on cancer cells.
{"title":"Influence of pteridines and statins on cancer: A therapeutic strategy targeting nitric oxide synthase (NOS) pathway","authors":"Jerimon Johnson , Monisha Krishnan , Sasireka Manikandan , Nivetha Shanmuganathan , Martinahingis Kennedy , Kris Santhiya Yeasuraj , Sridhar Muthusami , Angayarkanni Jayaraman","doi":"10.1016/j.arres.2026.100152","DOIUrl":"10.1016/j.arres.2026.100152","url":null,"abstract":"<div><div>A family of enzymes known as nitric oxide synthases (NOS) produces nitric oxide (NO), a tiny, unstable, and potentially hazardous gas that is highly diffusible across cell membranes. NO and NO metabolites, such as nitrite, nitrate, S-nitrosothiols, nitrosamines, and peroxynitrite, mediate a variety of cytotoxic and genotoxic effects, such as inhibition of mitochondrial respiration, protein and DNA damage that leads to gene mutation, loss of protein function, necrosis, and apoptosis. Through a variety of apoptotic mechanisms, abnormally elevated NO generation by NOS II/iNOS may cause cytotoxicity of cancer cells. Tetrahydrobiopterin (BH4) is required by all NOS isoforms for NO production. Another way mammalian cells can create BH4 is by the \"salvage pathway,\" which uses sepiapterin reductase and dihydrofolate reductase to convert sepiapterin to BH4. Better apoptotic effects on cancer cells may result from boosting BH4 levels by treating cells with sepiapterin, 7-8-dihydropterin, or pterin derivatives, which work in concert to improve NO levels. Another common medication used to treat and prevent hypercholesterolaemia and related cardiovascular disorders is statins, which lower serum cholesterol. They are competitive inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, the enzyme that limits the rate at which cholesterol is produced. Statins also improve cardiovascular and endothelial function by increasing the generation of nitric oxide (NO) by endothelial cells. They also have an impact on a variety of molecules and signaling pathways that govern the synthesis of apoptotic proteins and raise nitric oxide (NO) levels. Therefore, the NO-mediated route may be used to induce apoptosis due to the synergistic potency of statins and pterin derivatives. This review focusses on the effectiveness of statins and pterin derivatives, as well as their ability to influence the production of nitric oxide, which intensifies the effect on cancer cells.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100152"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-01DOI: 10.1016/j.arres.2026.100156
Wentao Li , Qi Jing , Qinjie Liu , Yi Yang , Jie Wu
Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation and oxidative stress, plays a pivotal role in intestinal pathophysiology. As the main site for iron absorption and a crucial barrier against environmental challenges, the intestinal epithelium is particularly vulnerable to oxidative stress and ferroptotic injury caused by iron overload. Emerging evidence highlights a complex interplay between gut microbiota, oxidative stress and ferroptosis, where pathogenic bacteria exacerbate ferroptosis through iron acquisition and oxidative stress induction, while beneficial microorganisms, particularly probiotics, offer protection by enhancing antioxidant defenses and modulating iron homeostasis. This review synthesizes current knowledge on the molecular mechanisms linking ferroptosis to intestinal diseases, with particular emphasis on dysregulated iron metabolism and redox imbalance in mucosal homeostasis. The bidirectional relationship between the gut microbiota and the regulation of ferroptosis is explored, highlighting key molecular mediators and signaling pathways. In addition, emerging therapeutic strategies targeting oxidative stress and ferroptosis are discussed, ranging from traditional iron chelation approaches to innovative interventions. The integration of these concepts offers valuable insights into the pathogenesis of intestinal diseases and suggests novel strategies for therapeutic development.
{"title":"Ferroptosis in gut pathophysiology: Molecular mechanisms and microbial regulation of iron metabolism and oxidative stress","authors":"Wentao Li , Qi Jing , Qinjie Liu , Yi Yang , Jie Wu","doi":"10.1016/j.arres.2026.100156","DOIUrl":"10.1016/j.arres.2026.100156","url":null,"abstract":"<div><div>Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation and oxidative stress, plays a pivotal role in intestinal pathophysiology. As the main site for iron absorption and a crucial barrier against environmental challenges, the intestinal epithelium is particularly vulnerable to oxidative stress and ferroptotic injury caused by iron overload. Emerging evidence highlights a complex interplay between gut microbiota, oxidative stress and ferroptosis, where pathogenic bacteria exacerbate ferroptosis through iron acquisition and oxidative stress induction, while beneficial microorganisms, particularly probiotics, offer protection by enhancing antioxidant defenses and modulating iron homeostasis. This review synthesizes current knowledge on the molecular mechanisms linking ferroptosis to intestinal diseases, with particular emphasis on dysregulated iron metabolism and redox imbalance in mucosal homeostasis. The bidirectional relationship between the gut microbiota and the regulation of ferroptosis is explored, highlighting key molecular mediators and signaling pathways. In addition, emerging therapeutic strategies targeting oxidative stress and ferroptosis are discussed, ranging from traditional iron chelation approaches to innovative interventions. The integration of these concepts offers valuable insights into the pathogenesis of intestinal diseases and suggests novel strategies for therapeutic development.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100156"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-02DOI: 10.1016/j.arres.2026.100150
Iman Mohammadi , Behzad Einollahi , Mina Alimohammadi , Seyedeh Mahdieh Khoshnazar , Hoda Sadeghi , Ali Zahiri , Haniye Najafzadeh , Kiavash Hushmandi
Background
Chronic and acute kidney disorders (CKD, AKI) afflict millions globally, leading to increased morbidity and death, especially from cardiovascular consequences. Atorvastatin, a popular statin, offers lipid-lowering, anti-inflammatory, and antioxidant qualities that may assist kidney disease patients in terms of renal and cardiovascular health. This meta-analysis assesses atorvastatin's effectiveness and safety in terms of lipid profiles, inflammatory biomarkers, and renal function in patients with kidney disorders.
Methods
A thorough search of Scopus, Cochrane, Embase, Web of Science, Google Scholar, and PubMed until January 2025 revealed randomized controlled trials (RCTs) evaluating atorvastatin in CKD, diabetic nephropathy, hemodialysis, and other renal diseases. The outcomes included lipid parameters (HDL, LDL, total cholesterol, triglycerides), inflammatory markers (hsCRP, IL-6, MDA), and renal function indices. Random-effects models were used to pool weighted mean differences (WMDs) and 95 % confidence intervals (CIs). Subgroup analyses were performed based on dosage, duration, disease type, and treatment type. The risk of bias and publication bias was evaluated.
Results
Twelve RCTs with 18 trials and sample sizes ranging from 21 to 156 participants were included. As expected, atorvastatin significantly improved HDL cholesterol (WMD: 2.74 mg/dL; 95 % CI: 0.57 to 4.91; p < 0.001) while dramatically decreasing LDL cholesterol (WMD: -13.09 mg/dL; 95 % CI: -21.17 to -5.00; p < 0.001) and total cholesterol (WMD: -15.28 mg/dL; 95 % CI: -24.58 to -5.98; p < 0.001) at lower dosages of ≤10 mg/day and longer treatment periods. More notably, it also reduced MDA (WMD: -2.80; 95 % CI: -3.62 to -1.97; p < 0.001) and showed anti-inflammatory effects by reducing hsCRP in CKD patients receiving a ≤ 10 mg/day dosage.
Conclusions
Atorvastatin medication improves lipid profiles and lowers oxidative stress indicators in renal disease patients, with some indications of decreased inflammation in select subgroups, indicating a possible function as an adjuvant treatment to reduce cardiovascular risk. Future large-scale RCTs are needed to determine the appropriate dose and long-term kidney results.
{"title":"The effect of atorvastatin on inflammatory markers, lipid profile, and renal function in kidney diseases: a systematic review and meta-analysis of randomized controlled trials","authors":"Iman Mohammadi , Behzad Einollahi , Mina Alimohammadi , Seyedeh Mahdieh Khoshnazar , Hoda Sadeghi , Ali Zahiri , Haniye Najafzadeh , Kiavash Hushmandi","doi":"10.1016/j.arres.2026.100150","DOIUrl":"10.1016/j.arres.2026.100150","url":null,"abstract":"<div><h3>Background</h3><div>Chronic and acute kidney disorders (CKD, AKI) afflict millions globally, leading to increased morbidity and death, especially from cardiovascular consequences. Atorvastatin, a popular statin, offers lipid-lowering, anti-inflammatory, and antioxidant qualities that may assist kidney disease patients in terms of renal and cardiovascular health. This meta-analysis assesses atorvastatin's effectiveness and safety in terms of lipid profiles, inflammatory biomarkers, and renal function in patients with kidney disorders.</div></div><div><h3>Methods</h3><div>A thorough search of Scopus, Cochrane, Embase, Web of Science, Google Scholar, and PubMed until January 2025 revealed randomized controlled trials (RCTs) evaluating atorvastatin in CKD, diabetic nephropathy, hemodialysis, and other renal diseases. The outcomes included lipid parameters (HDL, LDL, total cholesterol, triglycerides), inflammatory markers (hsCRP, IL-6, MDA), and renal function indices. Random-effects models were used to pool weighted mean differences (WMDs) and 95 % confidence intervals (CIs). Subgroup analyses were performed based on dosage, duration, disease type, and treatment type. The risk of bias and publication bias was evaluated.</div></div><div><h3>Results</h3><div>Twelve RCTs with 18 trials and sample sizes ranging from 21 to 156 participants were included. As expected, atorvastatin significantly improved HDL cholesterol (WMD: 2.74 mg/dL; 95 % CI: 0.57 to 4.91; <em>p</em> < 0.001) while dramatically decreasing LDL cholesterol (WMD: -13.09 mg/dL; 95 % CI: -21.17 to -5.00; <em>p</em> < 0.001) and total cholesterol (WMD: -15.28 mg/dL; 95 % CI: -24.58 to -5.98; <em>p</em> < 0.001) at lower dosages of ≤10 mg/day and longer treatment periods. More notably, it also reduced MDA (WMD: -2.80; 95 % CI: -3.62 to -1.97; <em>p</em> < 0.001) and showed anti-inflammatory effects by reducing hsCRP in CKD patients receiving <em>a</em> ≤ 10 mg/day dosage.</div></div><div><h3>Conclusions</h3><div>Atorvastatin medication improves lipid profiles and lowers oxidative stress indicators in renal disease patients, with some indications of decreased inflammation in select subgroups, indicating a possible function as an adjuvant treatment to reduce cardiovascular risk. Future large-scale RCTs are needed to determine the appropriate dose and long-term kidney results.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100150"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-06DOI: 10.1016/j.arres.2026.100151
Changchang Zhang , Xiao Yu , Peiji Li , Xiangmei Li , Jingwen Chen , Huan Wang , Mengying Yao
Acute Respiratory Distress Syndrome (ARDS) is a serious respiratory condition characterized by a rapid onset of severe inflammation in the lungs. This inflammation results from various causes. The syndrome is marked by widespread damage to the alveolar epithelial cells and capillary endothelial cells. It represents a critical stage of acute lung injury (ALI), a prevalent clinical issue associated with a high mortality rate. The underlying mechanisms of ALI are intricate and primarily driven by an uncontrolled inflammatory response. Given this complexity, there has been growing interest recently in the role of advanced glycation end-products (AGEs) and their receptor, the receptor for advanced glycation end-products (RAGE), in the development of ALI. The AGE-RAGE signaling pathway is pivotal in the initiation and progression of ALI, influencing several processes, including inflammation and apoptosis. However, the detailed mechanisms by which this signaling pathway contributes to ALI are still being investigated. This review aims to summarize recent advancements in understanding the molecular mechanisms, regulation of inflammatory responses, and apoptosis associated with the AGE-RAGE signaling pathway in ALI. It focuses on analyzing how various traditional Chinese medicine formulas and their active components can modulate this pathway to alleviate ALI. Additionally, by integrating network pharmacology, molecular docking, and experimental validation, this review examines the interactions between the AGE-RAGE signaling pathway and significant downstream pathways such as NF-κB and PI3K/AKT, highlighting their potential therapeutic implications. Therefore, this work provides a foundational understanding of the pathogenesis of ALI and paves the way for the development of innovative therapeutic approaches.
{"title":"Targeting the AGE-RAGE axis in acute lung injury: Mechanistic insights and redox-modulatory strategies","authors":"Changchang Zhang , Xiao Yu , Peiji Li , Xiangmei Li , Jingwen Chen , Huan Wang , Mengying Yao","doi":"10.1016/j.arres.2026.100151","DOIUrl":"10.1016/j.arres.2026.100151","url":null,"abstract":"<div><div>Acute Respiratory Distress Syndrome (ARDS) is a serious respiratory condition characterized by a rapid onset of severe inflammation in the lungs. This inflammation results from various causes. The syndrome is marked by widespread damage to the alveolar epithelial cells and capillary endothelial cells. It represents a critical stage of acute lung injury (ALI), a prevalent clinical issue associated with a high mortality rate. The underlying mechanisms of ALI are intricate and primarily driven by an uncontrolled inflammatory response. Given this complexity, there has been growing interest recently in the role of advanced glycation end-products (AGEs) and their receptor, the receptor for advanced glycation end-products (RAGE), in the development of ALI. The AGE-RAGE signaling pathway is pivotal in the initiation and progression of ALI, influencing several processes, including inflammation and apoptosis. However, the detailed mechanisms by which this signaling pathway contributes to ALI are still being investigated. This review aims to summarize recent advancements in understanding the molecular mechanisms, regulation of inflammatory responses, and apoptosis associated with the AGE-RAGE signaling pathway in ALI. It focuses on analyzing how various traditional Chinese medicine formulas and their active components can modulate this pathway to alleviate ALI. Additionally, by integrating network pharmacology, molecular docking, and experimental validation, this review examines the interactions between the AGE-RAGE signaling pathway and significant downstream pathways such as NF-κB and PI3K/AKT, highlighting their potential therapeutic implications. Therefore, this work provides a foundational understanding of the pathogenesis of ALI and paves the way for the development of innovative therapeutic approaches.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100151"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-11-26DOI: 10.1016/j.arres.2025.100145
Ahmed Abdulrazzaq Bapir , Burhan Ahmed Salih , Goran Othman
Background
Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disorder characterized by chronic hyperglycemia, oxidative stress, and low-grade inflammation. The CYP8B1 gene, a key regulator of bile acid synthesis and hepatic metabolism, may be influenced by oxidative status and has emerged as a potential contributor to T2DM pathogenesis. This study examined the association between CYP8B1 rs3732860 polymorphism, gene expression levels, and various biochemical and oxidative stress markers in individuals with T2DM.
Methods
A total of 198 subjects (132 T2DM patients and 66 healthy controls) were genotyped for the CYP8B1 rs3732860 variant. Biochemical parameters including HbA1c, glutathione peroxidase (GPX), catalase, malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-10 (IL-10), interferon-gamma (IFN-γ), and nitric oxide (NO) were measured. CYP8B1 expression was assessed using qPCR (ΔCt values). Statistical analyses included logistic regression, chi-square, ANOVA, and ROC curve analysis.
Results
The TC genotype was significantly associated with increased T2DM risk (OR = 4.51, 95 % CI: 1.85–11.01, p = 0.001), while the CC genotype showed a non-significant trend (OR = 2.25, p = 0.078). CYP8B1 expression differed significantly among genotypes (p < 0.001), with highest expression in CC carriers. MDA levels also varied by genotype (p = 0.001), suggesting a link between oxidative stress and gene regulation. ROC analysis identified catalase (AUC = 0.909) and SOD (AUC = 0.764) as strong predictors of T2DM.
Conclusion
The CYP8B1 rs3732860 polymorphism is associated with altered gene expression and oxidative stress in T2DM, highlighting its potential role as a metabolic regulator and biomarker of disease susceptibility.
{"title":"Association of CYP8B1 rs3732860 polymorphism and gene expression with oxidative stress and biochemical markers in Type 2 diabetes mellitus","authors":"Ahmed Abdulrazzaq Bapir , Burhan Ahmed Salih , Goran Othman","doi":"10.1016/j.arres.2025.100145","DOIUrl":"10.1016/j.arres.2025.100145","url":null,"abstract":"<div><h3>Background</h3><div>Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disorder characterized by chronic hyperglycemia, oxidative stress, and low-grade inflammation. The CYP8B1 gene, a key regulator of bile acid synthesis and hepatic metabolism, may be influenced by oxidative status and has emerged as a potential contributor to T2DM pathogenesis. This study examined the association between CYP8B1 rs3732860 polymorphism, gene expression levels, and various biochemical and oxidative stress markers in individuals with T2DM.</div></div><div><h3>Methods</h3><div>A total of 198 subjects (132 T2DM patients and 66 healthy controls) were genotyped for the CYP8B1 rs3732860 variant. Biochemical parameters including HbA1c, glutathione peroxidase (GPX), catalase, malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-10 (IL-10), interferon-gamma (IFN-γ), and nitric oxide (NO) were measured. CYP8B1 expression was assessed using qPCR (ΔCt values). Statistical analyses included logistic regression, chi-square, ANOVA, and ROC curve analysis.</div></div><div><h3>Results</h3><div>The TC genotype was significantly associated with increased T2DM risk (OR = 4.51, 95 % CI: 1.85–11.01, <em>p</em> = 0.001), while the CC genotype showed a non-significant trend (OR = 2.25, <em>p</em> = 0.078). CYP8B1 expression differed significantly among genotypes (<em>p</em> < 0.001), with highest expression in CC carriers. MDA levels also varied by genotype (<em>p</em> = 0.001), suggesting a link between oxidative stress and gene regulation. ROC analysis identified catalase (AUC = 0.909) and SOD (AUC = 0.764) as strong predictors of T2DM.</div></div><div><h3>Conclusion</h3><div>The CYP8B1 rs3732860 polymorphism is associated with altered gene expression and oxidative stress in T2DM, highlighting its potential role as a metabolic regulator and biomarker of disease susceptibility.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100145"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145694906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-04DOI: 10.1016/j.arres.2025.100147
Shiyu Liang , Youli Zhou , Wenfeng Ren , Yang Xu , Ming Tang , Yuxi Su , Li Li , Mei Gao
The Essential for Reactive Oxygen Species (EROS) protein, a critical molecular chaperone for NADPH oxidase 2 (NOX2/gp91phox), has emerged as a central regulator of redox signaling and immune defense. Recent structural and functional studies reveal that EROS orchestrates NOX2 maturation, prevents spontaneous activation, and regulates reactive oxygen species (ROS) production. Dysfunction of EROS is implicated in chronic granulomatous disease (CGD), cancers and vascular pathologies. This review integrates structural insights into EROS-NOX2 interactions, discusses its dual roles in maintaining redox equilibrium and triggering oxidative stress, and explores therapeutic strategies targeting EROS-dependent pathways.
{"title":"EROS protein: Decoding its pivotal role in redox homeostasis and disease pathogenesis","authors":"Shiyu Liang , Youli Zhou , Wenfeng Ren , Yang Xu , Ming Tang , Yuxi Su , Li Li , Mei Gao","doi":"10.1016/j.arres.2025.100147","DOIUrl":"10.1016/j.arres.2025.100147","url":null,"abstract":"<div><div>The Essential for Reactive Oxygen Species (EROS) protein, a critical molecular chaperone for NADPH oxidase 2 (NOX2/gp91<sup>phox</sup>), has emerged as a central regulator of redox signaling and immune defense. Recent structural and functional studies reveal that EROS orchestrates NOX2 maturation, prevents spontaneous activation, and regulates reactive oxygen species (ROS) production. Dysfunction of EROS is implicated in chronic granulomatous disease (CGD), cancers and vascular pathologies. This review integrates structural insights into EROS-NOX2 interactions, discusses its dual roles in maintaining redox equilibrium and triggering oxidative stress, and explores therapeutic strategies targeting EROS-dependent pathways.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100147"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145738770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-24DOI: 10.1016/j.arres.2026.100154
Darya Khalid Mahmood
Background
Tobacco use, whether through cigarettes or waterpipes, has been associated with the development of oxidative stress and a reduction in antioxidant defense. There is dearth of information on the impact of smoking frequency and duration among individuals of close age brackets. This study therefore aimed to assess salivary Total Antioxidant Capacity (TAOc) concentration among male dental students of different narrow age range with different smoking habits, including non-smokers, cigarette smokers, waterpipe users, and dual users.
Methods
In this cross-sectional study, 89 male dental students aged approximately 21.3 years were divided into four groups: non-smokers (n=14), cigarette smokers (n = 39), waterpipe users (n=11), and dual users (n=25). Smoking frequency and duration were recorded, and TAOc levels were measured. Data were analyzed using one-way ANOVA and post hoc Tukey tests.
Results
A significant difference in TAOc levels was observed among the four groups (P < 0.05). Non-smokers exhibited the highest antioxidant levels (27.93±3.79 U/ml), followed by waterpipe smokers (17.40±6.02 U/ml), cigarette smokers (15.59±7.45 U/ml), and dual users (9.68±6.89 U/ml). Post hoc analysis revealed that non-smokers had significantly higher TAOc levels compared to all smoking groups (P ≤ 0.001). Additionally, dual users had significantly lower TAOc than both single-type smokers. Smoking duration and frequency also influenced antioxidant levels, with a significant reduction observed in those with longer durations of use or higher frequency of smoking consumption.
Conclusion
Smoking, particularly dual use of cigarettes and waterpipes, is associated with a significant decline in salivary antioxidant capacity. Longer smoking duration and higher frequency further exacerbate this decline, highlighting the potential oxidative damage associated with tobacco use in young adults.
{"title":"Evaluation of salivary total antioxidant capacity in cigarette smokers versus water pipe smokers among dental students in Sulaimani city","authors":"Darya Khalid Mahmood","doi":"10.1016/j.arres.2026.100154","DOIUrl":"10.1016/j.arres.2026.100154","url":null,"abstract":"<div><h3>Background</h3><div>Tobacco use, whether through cigarettes or waterpipes, has been associated with the development of oxidative stress and a reduction in antioxidant defense. There is dearth of information on the impact of smoking frequency and duration among individuals of close age brackets. This study therefore aimed to assess salivary Total Antioxidant Capacity (TAOc) concentration among male dental students of different narrow age range with different smoking habits, including non-smokers, cigarette smokers, waterpipe users, and dual users.</div></div><div><h3>Methods</h3><div>In this cross-sectional study, 89 male dental students aged approximately 21.3 years were divided into four groups: non-smokers (n=14), cigarette smokers (<em>n</em> = 39), waterpipe users (n=11), and dual users (n=25). Smoking frequency and duration were recorded, and TAOc levels were measured. Data were analyzed using one-way ANOVA and post hoc Tukey tests.</div></div><div><h3>Results</h3><div>A significant difference in TAOc levels was observed among the four groups (<em>P</em> < 0.05). Non-smokers exhibited the highest antioxidant levels (27.93±3.79 U/ml), followed by waterpipe smokers (17.40±6.02 U/ml), cigarette smokers (15.59±7.45 U/ml), and dual users (9.68±6.89 U/ml). Post hoc analysis revealed that non-smokers had significantly higher TAOc levels compared to all smoking groups (<em>P</em> ≤ 0.001). Additionally, dual users had significantly lower TAOc than both single-type smokers. Smoking duration and frequency also influenced antioxidant levels, with a significant reduction observed in those with longer durations of use or higher frequency of smoking consumption.</div></div><div><h3>Conclusion</h3><div>Smoking, particularly dual use of cigarettes and waterpipes, is associated with a significant decline in salivary antioxidant capacity. Longer smoking duration and higher frequency further exacerbate this decline, highlighting the potential oxidative damage associated with tobacco use in young adults.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100154"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-27DOI: 10.1016/j.arres.2026.100155
Samir Dekali , Sabine François
Populations exposed to conflict and crisis zones - including military personnel, first responders, and civilians - face complex environmental stressors such as combustion-derived irritants, engineered nanoparticles, and ionizing radiation. Mitochondria, as central regulators of cellular bioenergetics and oxidative stress, are highly susceptible to these exposures. This review examines two key scenarios: (i) inhaled respiratory toxicants and (ii) radio-combined exposures involving nanoparticles and ionizing radiation. Both conditions converge on mitochondrial dysfunction, causing oxidative damage, disrupted energy metabolism, and long-term tissue impairment. We discuss how advanced 3D lung models and mitochondrial flux analyses provide mechanistic insight and enable the identification of mitochondria-targeted countermeasures, including antioxidants, biogenesis activators, and nanotherapeutics. In conflict and technological crisis settings, addressing mitochondrial vulnerability represents a pivotal opportunity to prevent chronic toxicity and reinforce physiological resilience across both military and civilian populations.
{"title":"Mitochondria at the frontline of environmental toxicity in conflict and crisis zones: mechanisms, models, and countermeasures","authors":"Samir Dekali , Sabine François","doi":"10.1016/j.arres.2026.100155","DOIUrl":"10.1016/j.arres.2026.100155","url":null,"abstract":"<div><div>Populations exposed to conflict and crisis zones - including military personnel, first responders, and civilians - face complex environmental stressors such as combustion-derived irritants, engineered nanoparticles, and ionizing radiation. Mitochondria, as central regulators of cellular bioenergetics and oxidative stress, are highly susceptible to these exposures. This review examines two key scenarios: (i) inhaled respiratory toxicants and (ii) radio-combined exposures involving nanoparticles and ionizing radiation. Both conditions converge on mitochondrial dysfunction, causing oxidative damage, disrupted energy metabolism, and long-term tissue impairment. We discuss how advanced 3D lung models and mitochondrial flux analyses provide mechanistic insight and enable the identification of mitochondria-targeted countermeasures, including antioxidants, biogenesis activators, and nanotherapeutics. In conflict and technological crisis settings, addressing mitochondrial vulnerability represents a pivotal opportunity to prevent chronic toxicity and reinforce physiological resilience across both military and civilian populations.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100155"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L-carnitine is a mitochondria-targeted compound that plays a pivotal role in lipid metabolism, redox balance, and inflammatory regulation, particularly under conditions of elevated metabolic demands such as exercise. This review explores the multifaceted functions of L-carnitine in modulating oxidative stress and inflammation, emphasizing its relevance to exercise physiology and clinical health. By facilitating the transport of long-chain fatty acids into mitochondria, L-carnitine enhances β-oxidation and energy production while buffering excess acetyl-CoA to maintain metabolic flexibility. Its antioxidant properties, mediated through the upregulation of SOD, GPx, and catalase, help mitigate reactive oxygen species (ROS) and preserve mitochondrial integrity. Concurrently, L-carnitine suppresses cytokines such as TNF-α and IL-6, interrupting the feedback loop between oxidative stress and chronic inflammation. These mechanisms are particularly beneficial during and after exercise, where L-carnitine supplementation has shown potential to improve endurance, reduce muscle damage, and accelerate recovery in some studies, although findings across the literature are not entirely consistent. Clinical evidence also supports its therapeutic potential in conditions like cardiovascular disease, non-alcoholic fatty liver disease, and neuroinflammation. The review integrates mechanistic insights with performance outcomes, highlighting L-carnitine’s role as both a metabolic modulator and an ergogenic aid. Understanding these complex interactions provides a foundation for optimizing L-carnitine use, yet further research is warranted to clarify the optimal form (e.g., LCLT, ALCAR), dosage, duration, and target populations to maximize its therapeutic and ergogenic potential.
{"title":"Role of L-carnitine in exercise training: Anti-inflammatory, antioxidant, and metabolic interactions","authors":"Soheil Aminizadeh , Aliasghar Zarezadehmehrizi , Maedeh Amiri Deh-Ahmadi , Beydolah Shahouzehi","doi":"10.1016/j.arres.2025.100149","DOIUrl":"10.1016/j.arres.2025.100149","url":null,"abstract":"<div><div>L-carnitine is a mitochondria-targeted compound that plays a pivotal role in lipid metabolism, redox balance, and inflammatory regulation, particularly under conditions of elevated metabolic demands such as exercise. This review explores the multifaceted functions of L-carnitine in modulating oxidative stress and inflammation, emphasizing its relevance to exercise physiology and clinical health. By facilitating the transport of long-chain fatty acids into mitochondria, L-carnitine enhances β-oxidation and energy production while buffering excess acetyl-CoA to maintain metabolic flexibility. Its antioxidant properties, mediated through the upregulation of SOD, GPx, and catalase, help mitigate reactive oxygen species (ROS) and preserve mitochondrial integrity. Concurrently, L-carnitine suppresses cytokines such as TNF-α and IL-6, interrupting the feedback loop between oxidative stress and chronic inflammation. These mechanisms are particularly beneficial during and after exercise, where L-carnitine supplementation has shown potential to improve endurance, reduce muscle damage, and accelerate recovery in some studies, although findings across the literature are not entirely consistent. Clinical evidence also supports its therapeutic potential in conditions like cardiovascular disease, non-alcoholic fatty liver disease, and neuroinflammation. The review integrates mechanistic insights with performance outcomes, highlighting L-carnitine’s role as both a metabolic modulator and an ergogenic aid. Understanding these complex interactions provides a foundation for optimizing L-carnitine use, yet further research is warranted to clarify the optimal form (e.g., LCLT, ALCAR), dosage, duration, and target populations to maximize its therapeutic and ergogenic potential.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100149"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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