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Antioxidants
Special Issues
Roles of Oxidative Stress in Human Pathophysiology
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Roles of Oxidative Stress in Human Pathophysiology

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: 30 September 2026 | Viewed by 2839

Special Issue Editor

Prof. Dr. Alexandros Georgakilas

E-Mail Website
Guest Editor
DNA Damage Laboratory, Physics Department, School of Applied Mathematical and Physical Sciences, National Technical University of Athens, Zografou Campus, 15780 Athens, Greece
Interests: radiation biology; cancer biology; DNA damage and repair; oxidative stress; carcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress, resulting from the imbalance between reactive oxygen/nitrogen species (ROS/RNS) and endogenous antioxidant defenses, plays a central role in shaping human pathology and pathophysiology. Due to constant pressure from endogenous and exogenous stressors (radiation, chemicals, pollution, microplastics, etc.), oxidative stress can contribute to molecular damage to DNA, proteins, and lipids, driving processes such as chronic inflammation, metabolic dysfunction, neurodegeneration, carcinogenesis, and loss of homeostasis. Understanding the dual nature of redox biology—as both a physiological regulator and a pathological trigger—remains a major challenge and an opportunity for therapeutic innovation.

This Special Issue of Antioxidants invites contributions that explore the diverse roles of oxidative stress across human diseases. We welcome original research articles, mechanistic studies, clinical investigations, and comprehensive reviews. Specific areas of interest include

  1. Oxidative stress in cancer biology, cardiovascular and metabolic disorders, and neurodegenerative diseases;
  2. Redox signaling and its dysregulation in human pathology;
  3. Biomarkers of oxidative stress and antioxidant capacity in clinical practice;
  4. Experimental and clinical evaluation of antioxidant therapies;
  5. Crosstalk amongoxidative stress, inflammation, and immune response;
  6. Translational and precision medicine approaches targeting redox balance.

By gathering cutting-edge research and perspectives, this Special Issue aims to advance our understanding of oxidative stress and foster new strategies for prevention, diagnosis, and treatment.

Prof. Dr. Alexandros Georgakilas
Guest Editor

Manuscript Submission Information

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • reactive oxygen species
  • redox signaling
  • antioxidants
  • inflammation
  • biomarkers
  • human diseases
  • therapy
  • pathology
  • pathophysiology

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Published Papers (4 papers)

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Research

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19 pages, 1118 KB  
Article
Systemic Oxidative and Nitrosative Stress in Benign Prostatic Hyperplasia
by Marek Biesiadecki, Sabina Galiniak, Krzysztof Balawender, Julia Połeć and Mateusz Mołoń
Antioxidants 2026, 15(4), 488; https://doi.org/10.3390/antiox15040488 - 14 Apr 2026
Viewed by 481
Abstract
Benign prostatic hyperplasia (BPH) is an age-related disorder increasingly linked to chronic inflammation and redox imbalance, yet its systemic oxidative and nitrosative profile remains insufficiently characterized. In this cross-sectional study, fasting serum samples were collected from 47 men with clinically confirmed BPH scheduled [...] Read more.
Benign prostatic hyperplasia (BPH) is an age-related disorder increasingly linked to chronic inflammation and redox imbalance, yet its systemic oxidative and nitrosative profile remains insufficiently characterized. In this cross-sectional study, fasting serum samples were collected from 47 men with clinically confirmed BPH scheduled for transurethral resection of the prostate and 40 healthy controls. We assessed antioxidant status (thiols, total antioxidant capacity), lipid peroxidation (malondialdehyde, 4-hydroxynonenal), protein nitration (3-nitrotyrosine), glycoxidation markers (Amadori products, advanced glycation end products (AGE)-associated fluorescence), and tryptophan metabolism indices (tryptophan, kynurenine, N′-formylkynurenine). Compared with controls, BPH patients showed significantly lower antioxidant capacity and thiol levels, together with increased lipid peroxidation and protein nitration. AGE-associated fluorescence was modestly elevated, whereas Amadori products and advanced oxidation protein products did not differ significantly. Tryptophan metabolism was markedly altered, with lower tryptophan and higher kynurenine and N′-formylkynurenine, indicating activation of the kynurenine pathway. After false discovery rate correction, most redox biomarkers remained significant. Multivariable logistic regression confirmed independent associations of lipid peroxidation, nitrosative stress, and kynurenine pathway activation with BPH after adjustment for age and metabolic parameters. These findings support a role for systemic oxidative and inflammatory mechanisms in BPH pathophysiology, although confirmation in age-matched and longitudinal studies is needed. Full article
(This article belongs to the Special Issue Roles of Oxidative Stress in Human Pathophysiology)
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Review

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39 pages, 2611 KB  
Review
Silent Inflammation: A Critical Narrative Review of the Relationship Between Periodontal Disease and Psychosis—The Role of Oxidative Stress and Iatrogenic Comorbidities
by Brindusa E. Focseneanu, Roxana M. Ciobanu, Anna M. Pangica, Petru T. Ionescu, Teodora M. Pangica, Gabriela Marian and Florentina C. Biclesanu
Antioxidants 2026, 15(6), 679; https://doi.org/10.3390/antiox15060679 - 28 May 2026
Abstract
Extensive epidemiological evidence links psychosis (PZ)—particularly schizophrenia (SCZ)—with disproportionate periodontal destruction, suggesting shared biological vulnerability. Beyond local tissue damage, periodontitis provides a clinically accessible translational paradigm for systemic redox dysregulation, where sustained inflammatory activation coincides with measurable oxidative injury and exhaustion of antioxidant [...] Read more.
Extensive epidemiological evidence links psychosis (PZ)—particularly schizophrenia (SCZ)—with disproportionate periodontal destruction, suggesting shared biological vulnerability. Beyond local tissue damage, periodontitis provides a clinically accessible translational paradigm for systemic redox dysregulation, where sustained inflammatory activation coincides with measurable oxidative injury and exhaustion of antioxidant (AO) defenses across cardiometabolic and neuropsychiatric domains. In this critical narrative review, we argue that the excess periodontal burden in PZ reflects a “pathological confluence” shaped by antipsychotic-associated iatrogenic factors, rapid metabolic deterioration, and chronic oxidative distress. We appraise the thioredoxin-interacting protein (TXNIP)–NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) axis as a metabolic–redox sensor linking dysglycemia to periodontal inflammasome activation and downstream cytokine signaling, and address the advanced glycation end-products (AGEs)–receptor for advanced glycation end-products (RAGE) axis as a key immunometabolic redox pathway. We further discuss mitochondrial dysfunction, impaired mitophagy, and mitochondrial deoxyribonucleic acid (mtDNA) leakage as damage-associated molecular patterns (DAMPs) that can amplify systemic “silent inflammation”. Integrating evidence on periodontal pathogen–host interactions and redox-sensitive neuroimmune pathways (including NADPH oxidase 4 (NOX4)-linked microglial activation), we propose periodontitis as a plausible upstream amplifier that may exacerbate vascular dysfunction and compromise blood–brain barrier (BBB) integrity. Finally, we outline clinically measurable biomarker readouts to operationalize redox-informed integrated care and highlight the need for pragmatic trials targeting clinically meaningful endpoints to improve somatic longevity in PZ-spectrum populations. We acknowledge that current human evidence is largely associative and that the proposed mechanistic links remain hypothesis generating. Full article
(This article belongs to the Special Issue Roles of Oxidative Stress in Human Pathophysiology)
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26 pages, 1127 KB  
Review
Redox Imbalance in the Cardiohepatic Syndrome: The Emerging Role of Oxidative Stress in Cirrhosis-Associated Cardiac Dysfunction
by Nikola Blagojevic, Dragana Blagojevic, Ana Matovic, Marko Cvrkotic, Marija Marjanovic-Haljilji, Aleksandra Sljivic, Ana Ilic, Natasa Cvetinovic, Irina Nenadic, Marko Djuric, Nemanja Dimic, Milica Aleksic, Jovana Bojicic, Aleksandra Djokovic, Snezana Lukic and Branka Filipovic
Antioxidants 2026, 15(4), 490; https://doi.org/10.3390/antiox15040490 - 15 Apr 2026
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Abstract
Cirrhosis is no longer viewed solely as an isolated hepatic disorder but rather as a complex multisystemic disease that affects cardiovascular, renal, pulmonary, metabolic, and immune systems. One of its most clinically relevant but under-recognized consequences is cardiac dysfunction, manifesting as cirrhotic cardiomyopathy, [...] Read more.
Cirrhosis is no longer viewed solely as an isolated hepatic disorder but rather as a complex multisystemic disease that affects cardiovascular, renal, pulmonary, metabolic, and immune systems. One of its most clinically relevant but under-recognized consequences is cardiac dysfunction, manifesting as cirrhotic cardiomyopathy, portopulmonary hypertension, right ventricular (RV) failure, and impaired myocardial strain. Oxidative stress (OS) has recently emerged as a fundamental mechanistic link between hepatic fibrogenesis and myocardial remodeling, acting through mitochondrial injury, NADPH oxidase activation, nitric oxide dysregulation, iron-mediated ferroptosis, and inflammatory cytokines. These alterations lead to diastolic dysfunction, autonomic imbalance, myocardial fibrosis, electrophysiological abnormalities (including QTc prolongation), and impaired RV–pulmonary artery coupling. Redox biomarkers such as malondialdehyde (MDA), NOX2-derived peptides, GSH/GSSG ratio, sST2, NT-proBNP, and 8-isoprostanes hold promise in detecting early subclinical cardiac involvement in cirrhosis. Novel antioxidant therapies, including mitochondrial-targeted molecules, NOX inhibitors, and ferroptosis blockers, may improve myocardial remodeling and hemodynamic stability. This review explores the central role of redox imbalance in the cardiohepatic syndrome and its potential utility in diagnosis, monitoring, and therapy. Full article
(This article belongs to the Special Issue Roles of Oxidative Stress in Human Pathophysiology)
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Other

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31 pages, 1716 KB  
Systematic Review
Salivary Oxidative Stress and Antioxidant Markers in Oral Leukoplakia: A Systematic Review and Meta-Analysis
by Patryk Wiśniewski, Magdalena Sulewska, Zuzanna Rybaczek, Kornelia Szymańska, Julia Nowakowska, Marcel Chrobot, Maja Podedworna, Karolina Doroszczyk, Paulina Murtaś and Małgorzata Pietruska
Antioxidants 2026, 15(2), 218; https://doi.org/10.3390/antiox15020218 - 6 Feb 2026
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Abstract
Oral leukoplakia (OL) is a common oral potentially malignant disorder in which chronic inflammation and carcinogenic exposures may promote oxidative stress. Saliva is in direct contact with the lesion and represents a non-invasive medium for assessing redox dysregulation. This systematic review and meta-analysis [...] Read more.
Oral leukoplakia (OL) is a common oral potentially malignant disorder in which chronic inflammation and carcinogenic exposures may promote oxidative stress. Saliva is in direct contact with the lesion and represents a non-invasive medium for assessing redox dysregulation. This systematic review and meta-analysis synthesized evidence on salivary oxidative damage markers and antioxidant defenses in OL compared with healthy controls. A PROSPERO-registered systematic review (CRD420251242238) was conducted in accordance with PRISMA and Cochrane guidelines. PubMed, Scopus and Web of Science were searched up to 10 December 2025 for observational studies comparing salivary oxidative stress and/or antioxidant markers in patients with clinically and/or histopathologically confirmed OL and healthy controls. Case–control and cross-sectional studies reporting quantitative data were included. Risk of bias was assessed using a modified Newcastle–Ottawa Scale. When ≥2 datasets were available, standardized mean differences (SMDs) with 95% confidence intervals (CI) were pooled. Meta-analysis showed significantly higher salivary malondialdehyde in OL (SMD = 1.47; 95% CI: 0.55–2.39), indicating enhanced lipid peroxidation. OL was also associated with significantly lower levels of reduced glutathione, vitamins C and E, and uric acid. For 8-hydroxy-2′-deoxyguanosine, a non-significant trend towards higher levels was observed with substantial heterogeneity. Evidence for TBARS, total antioxidant capacity and enzymatic antioxidants was limited. OL is associated with a salivary redox imbalance favoring a pro-oxidant state. High heterogeneity and limited biomarker-specific evidence highlight the need for larger, standardized prospective studies to validate salivary redox markers for OL monitoring and risk stratification. Full article
(This article belongs to the Special Issue Roles of Oxidative Stress in Human Pathophysiology)
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