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Oxidative Stress in Human Diseases—4th Edition

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (28 February 2026) | Viewed by 18928

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Dr. Soliman Khatib

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1. Department of Natural Products and Nutrition, MIGAL—Galilee Research Institute, Kiryat Shmona 11016, Israel 2. Faculty of Sciences, Tel Hai Academic College, Qiryat Shemona 12208, Israel
Interests: natural compounds; analytical chemistry; metabolomics; oxidative stress; atherosclerosis
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Dear Colleagues,

Oxidative stress (OS) is essential in the pathogenesis of human chronic diseases, such as cardiovascular and kidney diseases, diabetes, neurodegenerative disorders, cancer, inflammation-related diseases, and aging. OS is characterized by an imbalance between the production and accumulation of reactive oxygen and nitrogen species (ROS/RNS) in cells and tissues, and it occurs when the generation of these compounds exceeds the ability of the biological system to neutralize them.

ROS/RNS, such as superoxide (O₂^•−), hydrogen peroxide (H₂O₂), hydroxyl radical (HO^•), nitrogen oxide (NO^•), peroxynitrite (ONOO⁻), and hypochlorous acid (HOCl), are all products of normal metabolic pathways in humans; their production may increase as a result of influential external factors, such as pollution or cigarette smoke, or internally, as a result of impaired intracellular metabolism. Long-term exposure to increased levels of ROS/RNS can cause structural defects of lipids, proteins, DNA, and RNA, as well as functional alteration of several enzymes and cellular structures, leading to an increase in OS and pathogenesis.

We invite you to share your latest original and innovative research findings or review articles in this upcoming Special Issue, “Oxidative-Stress in Human Diseases—4th Edition”. We welcome clinical and pre-clinical studies on the relationship between OS and human diseases, novel diagnosis methods and mechanisms, and approaches to preventing and treating diseases related to OS.

Dr. Soliman Khatib
Guest Editor

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Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

oxidative stress
ROS/RNS
human diseases
antioxidants
OS biomarkers

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Published Papers (9 papers)

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Research

Jump to: Review

14 pages, 495 KB

Open AccessArticle

Elevated Amniotic Fluid 8-Iso-Prostaglandin F₂α Reveals Intrauterine Oxidative Stress in Fetuses with Congenital Heart Disease: A Prospective Case–Control Study

by Miguel Arráez, Marta Camprubí-Camprubí, María C. Escobar-Diaz, Laura Guirado, Laura Nogué, Mar Bennasar, Narcís Masoller, Fàtima Crispi, María Dolores Gómez-Roig, Olga Gómez and Míriam Pérez-Cruz

Antioxidants 2026, 15(5), 586; https://doi.org/10.3390/antiox15050586 - 6 May 2026

Viewed by 274

Abstract

Advances in prenatal diagnosis have improved the perinatal management of congenital heart disease (CHD). However postnatal comorbidities still persist due to multifactorial causes, which limits prenatal prediction of individual outcomes. Oxidative stress (OS), particularly lipid peroxidation, has been suggested to play a role in the development and progression of CHD, with 8-iso-prostaglandin F₂α (8-iso-PGF₂α) serving as a biomarker of oxidative injury. This prospective case–control study aimed to evaluate OS in fetuses with isolated major CHD by comparing amniotic fluid (AF) 8-iso-PGF₂α concentrations with controls. A total of 123 fetuses (83 CHD, 40 controls) were included at a tertiary CHD referral center. CHD cases were subclassified according to anatomical type and expected fetal brain perfusion under placental circulation. Controls were gestational age-matched pregnancies undergoing amniocentesis for indications unlikely to affect OS. All pregnant women underwent standardized fetal biometry, Doppler assessment, and detailed echocardiography. AF samples were obtained by amniocentesis and analyzed for free 8-iso-PGF₂α using a competitive ELISA, with values normalized to creatinine. Clinical, obstetric, and Doppler characteristics were comparable between groups. CHD fetuses showed significantly higher AF 8-iso-PGF₂α concentrations than controls (2849 ± 1377 vs. 2088 ± 1087 ng/mg Cr, p = < 0.001), and remained significant after adjustment for GA, smoking status, diabetes and maternal age and body mass index (BMI). No consistent differences were observed across anatomical or hemodynamic CHD subgroups. These findings provide the first intrauterine evidence of increased lipid peroxidation in fetuses with CHD as reflected by elevated amniotic fluid 8-iso-PGF₂α concentrations. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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20 pages, 1587 KB

Open AccessArticle

Loss of ABCC6 in Human Mesenchymal Stem Cells Leads to Elevated Reactive Oxygen Species Formation and a Senescence-like Phenotype

by Michel R. Osterhage, Cornelius Knabbe and Doris Hendig

Antioxidants 2026, 15(2), 241; https://doi.org/10.3390/antiox15020241 - 12 Feb 2026

Viewed by 582

Abstract

Pseudoxanthoma elasticum (PXE) is an autosomal-recessive disorder caused by mutations in ATP-binding cassette subfamily C member 6 (ABCC6). In addition to the calcification and fragmentation of elastic fibers as the pathomechanistic cause of PXE, systemic and cellular oxidative stress have been reported. Human mesenchymal stem cells (hMSCs) with an ABCC6 knockdown were chosen to further investigate the oxidative stress associated with ABCC6 deficiency. The cells were treated with hydrogen peroxide to mimic external oxidative stress and the antioxidant Trolox to examine the cells’ reaction to decreased oxidative stress. The level of different types of reactive species (RS) like nitric oxide and reactive oxygen species, the senescent phenotype, oxidative damage and mRNA expression of oxidative stress-related genes were evaluated. Knockdown of ABCC6 was shown to increase RS levels in hMSCs, induce a p53-dependent senescence-like phenotype and increase oxidative damage, while the mRNA expression of oxidative defense genes was elevated. The ABCC6-deficient cells exhibited an altered reaction to additional oxidative stress and the incubation with Trolox reversed these changes induced by ABCC6 knockdown. Our findings provide further evidence linking ABCC6-deficiency to oxidative stress and a senescence-like phenotype, while pointing towards antioxidants as part of a potential treatment for PXE. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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20 pages, 2773 KB

Open AccessArticle

Plasma, Urinary, and Salivary Total Redox Status in Critically Ill Patients with Brain Injury and Secondary Organ Failure

by Ewa Rynkiewicz-Szczepanska, Urszula Kosciuczuk, Katarzyna Anikiej, Anna Zalewska, Małgorzata Żendzian-Piotrowska and Mateusz Maciejczyk

Antioxidants 2026, 15(2), 185; https://doi.org/10.3390/antiox15020185 - 2 Feb 2026

Viewed by 689

Abstract

Little is known about the clinical utility of blood, salivary, and urinary redox biomarkers in critically ill patients with brain injury and secondary organ failure. The aim of the study was to explore total antioxidant and oxidant status in neurocritically ill patients using ferric reducing antioxidant power (FRAP), total antioxidant capacity (TAC), and total oxidant status (TOS) in plasma, saliva, and urine from the study (n = 45) and the healthy control group (n = 49). We analyzed the relationship between well-known biomarkers of organ function and redox status in different biofluids. Plasma FRAP was significantly higher (p < 0.05), but salivary and urinary FRAP were statistically lower in the study group (p < 0.05, p < 0.001) compared with controls. The salivary and urinary TAC were statistically lower (p < 0.05, p < 0.001), while plasma TOS was significantly higher (p < 0.05) in the study group compared with the control group. Circulating redox status did not differ between survivors and non-survivors. Significant associations were observed in non-survivors: salivary TAC correlated with urea and creatinine; salivary FRAP with creatinine, troponin, and CRP; urinary TAC with troponin and P_aO₂/FiO₂ ratio, as well as plasma FRAP with P_aO₂/FiO₂ ratio. The plasma FRAP had a significant effect on survival (AUC = 0.687, p = 0.02), with 69% sensitivity and 83% specificity. Crucial differences in redox status in blood, saliva, and urine were observed between neurocritically ill patients and healthy controls; however, none of the biomarkers differed between survivors and non-survivors. Oxidative and antioxidant status correlated with organ function in non-survivors. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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18 pages, 8983 KB

Open AccessArticle

Weizmannia coagulans BC179 Alleviates Post-Alcohol Discomfort May via Taurine-Related Metabolism and Antioxidant Regulation: A Randomized, Double-Blind, Placebo-Controlled Trial

by Mengyao Duan, Ying Wu, Jie Zhang, Saman Azeem, Yao Dong, Zhonghui Gai, Jianguo Zhu, Shuguang Fang and Shaobin Gu

Antioxidants 2025, 14(9), 1038; https://doi.org/10.3390/antiox14091038 - 23 Aug 2025

Cited by 1 | Viewed by 2222

Abstract

Excessive alcohol consumption is associated with various health complications, including liver damage and systemic inflammation. Probiotic interventions have emerged as promising strategies to mitigate alcohol-induced harm, yet their mechanisms of action remain incompletely understood. This randomized, double-blind, placebo-controlled clinical trial aimed to evaluate the protective effects of Weizmannia coagulans BC179 in chronic alcohol consumers. Seventy participants with a history of long-term alcohol intake were randomly assigned to receive either BC179 (3 g/day, 1 × 10¹⁰ CFU) or a placebo for a 30-day intervention period. Following alcohol ingestion, dynamic monitoring of blood alcohol concentration (BAC), inflammatory and oxidative stress biomarkers, and serum metabolomic profiles was conducted. BC179 supplementation significantly reduced BAC and enhanced the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), while decreasing levels of alkaline phosphatase (ALP), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Conversely, the anti-inflammatory cytokine interleukin-10 (IL-10), superoxide dismutase (SOD), and glutathione (GSH) were significantly upregulated. Levels of cytochrome P4502E1 (CYP2E1) and malondialdehyde (MDA) were also markedly reduced. Metabolomic analysis revealed significant modulation of taurine and hypotaurine metabolism, as well as downregulation of caffeine-related pathways. Collectively, these findings indicate that W. coagulans BC179 alleviates alcohol-induced discomfort by enhancing alcohol metabolism, attenuating inflammation, reducing oxidative stress, and modulating key metabolic pathways. This probiotic strain may represent a promising adjunctive strategy for managing alcohol-related health issues. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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12 pages, 1547 KB

Open AccessArticle

Effects of Photodynamic Therapy and Glucocorticosteroids on Salivary Oxidative Stress in Oral Lichen Planus: A Randomized Clinical Trial

by Patryk Wiśniewski, Magdalena Sulewska, Jagoda Tomaszuk, Anna Zalewska, Sara Zięba, Aleksandra Pietruska, Emilia Szymańska, Katarzyna Winnicka, Mateusz Maciejczyk, Małgorzata Żendzian-Piotrowska and Małgorzata Pietruska

Antioxidants 2025, 14(8), 1017; https://doi.org/10.3390/antiox14081017 - 20 Aug 2025

Cited by 6 | Viewed by 1873

Abstract

Objective: This study aimed to assess the impact of photodynamic therapy (PDT) and topical glucocorticosteroids (GKS) on total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI) in the saliva of patients with oral lichen planus (OLP). Methods: Ninety patients with histopathologically confirmed OLP were randomly assigned to either the PDT group (n = 50) or the GKS group (n = 40). Unstimulated saliva samples were collected before treatment and at 1, 3, and 6 months post-therapy. TOS, TAC, and OSI were determined using colorimetric assays. Results: Both PDT and GKS significantly reduced TOS over the entire observation period. TAC decreased persistently after GKS but remained stable after PDT except for an initial decline. OSI was significantly lower immediately after PDT but did not show sustained differences. Overall, PDT more effectively and durably restored redox balance compared to GKS. Conclusions: Photodynamic therapy demonstrates superior long-term efficacy in modulating oxidative stress markers in saliva, supporting its role as a promising alternative to topical corticosteroids in managing OLP. Clinically, these findings suggest that PDT may offer a non-invasive, recurrence-reducing, and steroid-sparing treatment alternative for OLP, potentially improving long-term patient outcomes and reducing side effects associated with prolonged corticosteroid use. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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Review

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46 pages, 2018 KB

Open AccessReview

The Role of Se-Containing Glutathione Peroxidases and Thioredoxin Reductases in Oncogenesis: Expression Paradoxes and Therapeutic Prospects

by Elena G. Varlamova, Sergey V. Gudkov and Egor A. Turovsky

Antioxidants 2026, 15(3), 312; https://doi.org/10.3390/antiox15030312 - 1 Mar 2026

Cited by 1 | Viewed by 1440

Abstract

This review synthesizes current evidence on the dualistic and context-dependent roles of selenium-containing antioxidant enzymes—specifically, glutathione peroxidases (GPXs) and thioredoxin reductases (TXNRDs)—in the development and progression of human cancers. We analyze how these crucial components of cellular redox homeostasis can function as either potent oncogenes or tumor suppressors depending on the tissue of origin, cancer stage, genetic background, and tumor microenvironment. The paradoxical behavior of these enzymes is governed by a complex interplay of transcriptional regulation, epigenetic modifications, and signaling pathway interactions, ultimately influencing critical processes such as apoptosis, proliferation, invasion, and therapy resistance. Special emphasis is placed on the unique role of GPX4 in regulating ferroptosis, a promising target for novel anti-cancer strategies, and on the prognostic significance of TXNRD overexpression in aggressive malignancies. By integrating data across various cancer types, this review highlights these enzyme families as central molecular switches in carcinogenesis and discusses their potential as biomarkers and targets for rational, combination-based therapeutic interventions. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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31 pages, 1218 KB

Open AccessReview

Current Insights into Glutathione Depletion in Adult Septic Patients

by Sonia Gomar, Ricardo Bou, Francisco Javier Puertas, María Miranda, Francisco Javier Romero and Belén Romero

Antioxidants 2025, 14(9), 1033; https://doi.org/10.3390/antiox14091033 - 22 Aug 2025

Cited by 8 | Viewed by 2978

Abstract

Sepsis is a complex condition characterized by an uncontrolled inflammatory response to infection, which can trigger multi-organ dysfunction and is associated with high mortality rates. In this context, oxidative stress plays a key role in the progression of tissue damage. Reduced glutathione (GSH), the primary non-enzymatic intracellular antioxidant, serves as a fundamental pillar in redox defense, acting as a key modulator of immune response, endothelial barrier integrity, and mitochondrial metabolism. This review explores the multifaceted role of GSH in the pathophysiology of sepsis, with emphasis on its biphasic effect on both innate and adaptive immunity, as well as its involvement in vascular alterations and mitochondrial dysfunction. The molecular mechanisms of GSH depletion during sepsis are analyzed, including excessive consumption by reactive species, disruption of its synthesis, and its intracellular compartmentalization. Additionally, the available clinical evidence in humans regarding the functional consequences of GSH loss is reviewed, particularly concerning organ failure—understood more as a bioenergetic and functional disruption than a structural one—and mortality, highlighting the methodological limitations and heterogeneity of the reported findings. Altogether, this analysis intends to provide a comprehensive view of the role of glutathione in redox dysregulation and the pathophysiological mechanisms underlying sepsis. Furthermore, it seeks to consolidate current pathophysiological and clinical knowledge to emphasize the potential role of glutathione as a prognostic marker and possible target for future therapeutic strategies in addressing this complex condition. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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19 pages, 2360 KB

Open AccessReview

Antioxidant Effects of SGLT2 Inhibitors on Cardiovascular–Kidney–Metabolic (CKM) Syndrome

by Juan Guerrero-Mauvecin, Natalia Villar-Gómez, Lucia Miño-Izquierdo, Adrián Povo-Retana, Adrian M. Ramos, Gema Ruiz-Hurtado, Maria D. Sanchez-Niño, Alberto Ortiz and Ana B. Sanz

Antioxidants 2025, 14(6), 701; https://doi.org/10.3390/antiox14060701 - 9 Jun 2025

Cited by 8 | Viewed by 4644

Abstract

The cardiovascular–kidney–metabolic (CKM) syndrome was recently conceptualized to provide a holistic framework for diagnosing and treating the full spectrum of key age-associated interrelated conditions: overweight/obesity, type 2 diabetes mellitus, acute and chronic kidney disease, and cardiovascular disease. This conceptualization resulted from epidemiological associations, advances in our understanding of shared and interrelated pathogenic mechanisms, and observations that several drug families improved outcomes in all three components of CKM. Sodium/glucose cotransporter 2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP-1 RA) enhance all CKM spectrum components, although their efficacy varies against specific components. However, the modified mechanisms by these drugs beyond glycemic control in CKM syndrome are poorly understood. We now deeply review the available literature regarding the impact of SGLT2i on oxidative stress and antioxidant defenses in preclinical and clinical studies of type 2 diabetes mellitus, acute and chronic kidney disease, cardiovascular disease, and CKM syndrome. Evidence suggests that SGLT2i may have a secondary antioxidant effect that reduces the vicious cycle of tissue injury—inflammation—tissue injury, even in organs distant from the primary injury. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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20 pages, 2577 KB

Open AccessReview

The Potential Role of Oxidative Stress in Modulating Airway Defensive Reflexes

by Yuki Sato, Yoichiro Sugiyama, Tomoya Ishida, Haruhiko Inufusa, Fukka You, Davis Joseph and Shigeru Hirano

Antioxidants 2025, 14(5), 568; https://doi.org/10.3390/antiox14050568 - 9 May 2025

Cited by 4 | Viewed by 3139

Abstract

Airway defensive reflexes, such as pharyngeal swallowing, coughing, and sneezing, play a pivotal role in maintaining airway homeostasis. These reflexes are controlled by complex mechanisms primarily governed by specific neuronal circuitry in the brainstem, referred to as central pattern generators. These behaviors also require optimal conditions for the peripheral organs within the airway and alimentary tracts, including the nose, pharynx, larynx, and trachea, which are vital for ensuring appropriate responsiveness and motor outputs. Oxidative stress is linked to the development and progress of impaired functions of those behaviors. Dysphagia caused by central or peripheral impairments, such as neurodegeneration of related neuronal networks and laryngeal desensitization, is likely associated with an increased level of oxidative stress. Chronic inflammation and allergic airway sensitization in the lower airways, including asthma, elevate oxidative stress levels and diminish the activity of antioxidant defense enzymes, which exacerbate the severity of respiratory conditions. Antioxidant supplements offer promising therapeutic benefits by facilitating the recovery of distorted airway defensive reflexes, although limited information has been provided concerning therapeutic strategies. Further studies are necessary to enhance our understanding of the pathophysiology of dysphagia and airway diseases related to oxidative stress, as well as to develop new treatment strategies for these disorders. Full article

(This article belongs to the Special Issue Oxidative Stress in Human Diseases—4th Edition)

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