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Exploring Biomarkers of Oxidative Stress in Health and Disease

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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 (31 August 2025) | Viewed by 10328

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Special Issue Editors

Prof. Dr. Daniela Gradinaru

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Department of Biochemistry, Faculty of Pharmacy, Carol Davila University of Medicine and Pharmacy, 020956 Bucharest, Romania
Interests: oxidative stress; cardiometabolic diseases; ageing; lipoprotein metabolism; drug metabolism; geroprotectors

Prof. Dr. Denisa Marilena Margină

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Guest Editor

Department of Biochemistry, Faculty of Pharmacy, Carol Davila University of Medicine and Pharmacy, 020956 Bucharest, Romania
Interests: natural compounds; oxidative stress; inflammation; metabolic disease; diabetes; aging
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Dear Colleagues,

For forty decades, the concept of oxidative stress has remained an important focus of interest in biomedical research, and limiting oxidative stress intensity became a cutting-edge therapeutic goal of pharmaceutical research. This imbalance in redox homeostasis and the consequent oxidative damage accumulation in macromolecules has been considered as a cause of cellular impairment, being associated with numerous risk factors of several diseases, with age-related pathological conditions as well as with normal ageing. This continuous interest in oxidative stress is also highlighted by the development of new molecules, such as dimethyl fumarate, that act through signalling pathways modulating redox homeostasis (e.g., Nrf2) and that are used as targeted therapy against severe diseases (multiple sclerosis).

In this Special Issue, the main emphasis will be on the relevance of oxidative stress biomarkers assessed under specific physiopathological/toxicological situations such as metabolic dysregulations (dyslipidaemia, chronic hyperglycaemia, hyperinsulinaemia, hyperuricaemia), intoxications, or environmental exposure to harmful agents (cigarette smoking, pollutants, UV and ionizing irradiation). This approach is necessary since redox imbalance pathways and oxidative stress biomarkers are studied extensively and considered as new targets in prevention, diagnosis and therapy for cardiometabolic diseases (cardiovascular diseases, type 2 diabetes mellitus, metabolic syndrome and obesity), neurodegenerative disorders, cancer, inflammation, and also as candidate biomarkers in evaluating the human biological age.

We invite investigators to contribute with critical reviews and original research articles concerning the most recent advances in the study of oxidative stress biomarkers which emerged as relevant tools for the investigation and diagnosis of oxidopathies and for monitoring the efficiency of antioxidant therapies in clinical samples or experimental models.

Potential topics include, but are not limited to, the following:

Lipid and lipoprotein oxidation markers;
Protein oxidation and glycoxidation;
Protein carbonylation, nitration and chlorination;
Protein glutathionylation;
DNA/RNA oxidative damage;
Enzymatic and non-enzymatic antioxidant defence;
Antioxidant status/properties;
Redox cellular/molecular pathways.

Prof. Dr. Daniela Gradinaru
Prof. Dr. Denisa Marilena Margină
Guest Editors

Manuscript Submission Information

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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 and nitrosative stress
AGEs—advanced glycation end-products
lipid peroxidation
nitrotyrosine
glutathione
8-oxo-2'-deoxyguanosine
inflammation
cardiometabolic risk
cancer
neurodegeneration
nanoparticles
xenobiotic
antioxidant
ageing
advanced therapies

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Published Papers (8 papers)

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Research

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15 pages, 14322 KB

Open AccessArticle

Clinical Evaluation of Oxidative Stress Markers in Patients with Long COVID During the Omicron Phase in Japan

by Osamu Mese, Yuki Otsuka, Yasue Sakurada, Kazuki Tokumasu, Yoshiaki Soejima, Satoru Morita, Yasuhiro Nakano, Hiroyuki Honda, Akiko Eguchi, Sanae Fukuda, Junzo Nojima and Fumio Otsuka

Antioxidants 2025, 14(9), 1068; https://doi.org/10.3390/antiox14091068 - 30 Aug 2025

Viewed by 697

Abstract

To characterize changes in markers of oxidative stress for the clinical evaluation of patients with long COVID, we assessed oxidative stress and antioxidant activity based on serum samples from patients who visited our clinic between May and November 2024. Seventy-seven patients with long COVID (41 [53%] females and 36 [47%] males; median age, 44 years) were included. Median [interquartile range] serum levels of diacron-reactive oxygen metabolites (d-ROM; CARR Unit), biological antioxidant potential (BAP; μmol/L), and oxidative stress index (OSI) were 533.8 [454.9–627.6], 2385.8 [2169.2–2558.1] and 2.0 [1.7–2.5], respectively. Levels of d-ROMs (579.8 vs. 462.2) and OSI (2.3 vs. 1.8), but not BAP (2403.4 vs. 2352.6), were significantly higher in females than in males. OSI levels positively correlated with age and body mass index, whereas BAP levels negatively correlated with these parameters. d-ROM and OSI levels were significantly associated with inflammatory markers, including C-reactive protein (CRP) and fibrinogen, whereas BAP levels were inversely correlated with CRP and ferritin levels. Notably, serum free thyroxine levels were negatively correlated with d-ROMs and OSI, whereas cortisol levels were positively correlated with d-ROMs. Among long COVID symptoms, patients reporting brain fog exhibited significantly higher OSI levels (2.2 vs. 1.8), particularly among females (d-ROMs: 625.6 vs. 513.0; OSI: 2.4 vs. 2.0). The optimal OSI cut-off values were determined to be 1.32 for distinguishing long COVID from healthy controls and 1.92 for identifying brain fog among patients with long COVID. These findings suggest that oxidative stress markers may serve as indicators for the presence or prediction of psycho-neurological symptoms associated with long COVID in a gender-dependent manner. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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19 pages, 1021 KB

Open AccessArticle

Causal Inference Approaches Reveal Associations Between LDL Oxidation, NO Metabolism, Telomere Length and DNA Integrity Within the MARK-AGE Study

by Andrei Valeanu, Denisa Margina, María Moreno-Villanueva, María Blasco, Ewa Sikora, Grazyna Mosieniak, Miriam Capri, Nicolle Breusing, Jürgen Bernhardt, Christiane Schön, Olivier Toussaint, Florence Debacq-Chainiaux, Beatrix Grubeck-Loebenstein, Birgit Weinberger, Simone Fiegl, Efstathios S. Gonos, Antti Hervonen, Eline P. Slagboom, Anton de Craen, Martijn E. T. Dollé, Eugène H. J. M. Jansen, Eugenio Mocchegiani, Robertina Giacconi, Francesco Piacenza, Marco Malavolta, Daniela Weber, Wolfgang Stuetz, Tilman Grune, Claudio Franceschi, Alexander Bürkle and Daniela Gradinaru Show full author list Hide full author list

Antioxidants 2025, 14(8), 933; https://doi.org/10.3390/antiox14080933 - 30 Jul 2025

Viewed by 598

Abstract

Genomic instability markers are important hallmarks of aging, as previously evidenced within the European study of biomarkers of human aging, MARK-AGE; however, establishing the specific metabolic determinants of vascular aging is challenging. The objective of the present study was to evaluate the impact of the susceptibility to oxidation of serum LDL particles (LDLox) and the plasma metabolization products of nitric oxide (NOx) on relevant genomic instability markers. The analysis was performed on a MARK-AGE cohort of 1326 subjects (635 men and 691 women, 35–75 years old) randomly recruited from the general population. The Inverse Probability of Treatment Weighting causal inference algorithm was implemented in order to assess the potential causal relationship between the LDLox and NOx octile-based thresholds and three genomic instability markers measured in mononuclear leukocytes: the percentage of telomeres shorter than 3 kb, the initial DNA integrity, and the DNA damage after irradiation with 3.8 Gy. The results showed statistically significant telomere shortening for LDLox, while NOx yielded a significant impact on DNA integrity. Overall, the effect on the genomic instability markers was higher than for the confirmed vascular aging determinants, such as low HDL cholesterol levels, indicating a meaningful impact even for small changes in LDLox and NOx values. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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18 pages, 1717 KB

Open AccessArticle

An Immune Assay to Quantify the Neutralization of Oxidation-Specific Epitopes by Human Blood Plasma

by Marija Jelic, Philipp Jokesch, Olga Oskolkova, Gernot Faustmann, Brigitte M. Winklhofer-Roob, Bernd Ullrich, Jürgen Krauss, Rudolf Übelhart, Bernd Gesslbauer and Valery Bochkov

Antioxidants 2025, 14(8), 903; https://doi.org/10.3390/antiox14080903 - 24 Jul 2025

Viewed by 542

Abstract

Oxidized phospholipids (OxPLs) are increasingly recognized as biologically active lipids involved in various pathologies. Both exposure to pathogenic factors and the efficacy of protective mechanisms are critical to disease development. In this study, we characterized an immunoassay that quantified the total capacity of the plasma to degrade or mask OxPLs, thereby preventing their interaction with cells and soluble proteins. OxLDL-coated plates were first incubated with human blood plasma or a control vehicle, followed by an ELISA using a monoclonal antibody specific to oxidized phosphatidylethanolamine. Pretreatment with the diluted blood plasma markedly inhibited mAb binding. The masking assay was optimized by evaluating the buffer composition, the compatibility with various anticoagulants, potential interfering compounds, the kinetic parameters, pre-analytical stability, statistical robustness, and intra- and inter-individual variability. We propose that this masking assay provides a simple immunological approach to assessing protective mechanisms against lipid peroxidation products. Establishing this robust and reproducible method is essential for conducting clinical association studies that explore masking activity as a potential biomarker of the predisposition to a broad range of lipid-peroxidation-related diseases. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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13 pages, 554 KB

Open AccessArticle

Genetic Variants in Antioxidant Genes Modulate the Relationships Among Obesity-Related Oxidative Stress Markers in Mexican Children

by Ana Nava-Cabrera, Armando Ramírez-Cruz, Jaime Gómez-Zamudio, Araceli Pérez-Bautista, Linda Esther Ruiz-Queb, Miguel Vazquez-Moreno and Miguel Cruz

Antioxidants 2025, 14(8), 896; https://doi.org/10.3390/antiox14080896 - 22 Jul 2025

Viewed by 499

Abstract

Single-nucleotide polymorphisms (SNPs) in antioxidant genes could influence redox regulation from early life. We aimed to assess the direct and modulatory effects of SNPs in antioxidant genes (SOD2 rs4880, GPX1 rs1050450, GPX7 rs835337, CAT rs1001179) on the relationships among obesity-related oxidative stress markers in Mexican children. Anthropometric data of 2946 unrelated children were analyzed in this cross-sectional study. SNPs were genotyped using TaqMan assay. Serum total antioxidant capacity (sTAC) and oxidative stress markers (thiobarbituric acid reactive substances [TBARS, as lipid peroxidation], and protein carbonyl [PC]) were assessed. Although no SNPs were associated with obesity (p ≥ 0.125), both sTAC (p = 0.001) and TBARS (p = 0.015) were positively associated with it. A negative relationship was also observed between sTAC and TBARS (p < 0.001). SOD2 rs4880 was negatively associated with TBARS, while GPX1 rs1050450 was inversely associated with both TBARS and PC levels (p ≤ 0.036). The inverse association between sTAC and TBARS remained significant only in non-carriers of SOD2 rs4880 (p = 0.003) and GPX1 rs1050450 (p = 0.002). Our data evidence that sTAC and TBARS are associated with obesity, showing a negative relationship in Mexican children who are non-carriers of SOD2 rs4880 and GPX1 rs1050450. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

20 pages, 16827 KB

Open AccessArticle

Selenium-Binding Protein 1-Deficient Dendritic Cells Protect Mice from Sepsis by Increased Treg/Th17

by Xin Zhang, Shuang Han, Zhu Zeng, Jie Dai and Yi Jia

Antioxidants 2025, 14(4), 468; https://doi.org/10.3390/antiox14040468 - 14 Apr 2025

Viewed by 915

Abstract

Selenium-binding protein 1 (SELENBP1) has been implicated in cancer development, neurological disorders, tissue injury, metabolic regulation, and cell differentiation. Sepsis is characterized prominently by immunological dysregulation and severe organ damage. However, whether SELENBP1 improves sepsis by regulating immune cell activity remains unknown. Here, we detected an elevation of SELENBP1 levels in the blood of sepsis patients and in the livers of septic mice. Significantly, SELENBP1 knockout (KO) prolonged survival in septic mice. This phenomenon was accompanied by decreased liver damage, reduced inflammation levels, and an increased regulatory T cell/T helper 17 cell (Treg/Th17) ratio in the spleen. Additionally, SELENBP1 deficiency induced a redox imbalance and inhibited dendritic cell (DC) maturation, resulting in a tolerogenic DC (tolDC) phenotype and an increase in the Treg/Th17 ratio. Furthermore, SELENBP1-KO mature DCs (mDCs) alleviated liver injury by increasing the Treg/Th17 ratio in the spleen, thus improving the survival of septic mice. These findings indicate that SELENBP1 is involved in sepsis by regulating DC immune activity, which might provide a potential way for sepsis treatment. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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14 pages, 1512 KB

Open AccessArticle

Pattern of Expression of Genes Involved in Systemic Inflammation and Glutathione Metabolism Reveals Exacerbation of COPD

by Ingrid Oit-Wiscombe, László Virág, Kalle Kilk, Ursel Soomets and Alan Altraja

Antioxidants 2024, 13(8), 953; https://doi.org/10.3390/antiox13080953 - 6 Aug 2024

Cited by 2 | Viewed by 1514

Abstract

To test the hypothesis that they serve as systemic biomarkers of chronic obstructive pulmonary disease (COPD), we profiled the mRNA expression of enzymes connected to systemic inflammation and GSH metabolism in peripheral blood mononuclear cells (PBMCs). These were taken from patients displaying acute exacerbation of COPD (AE-COPD) and stable COPD, and also from non-obstructive smokers and non-smokers. The expression of poly(ADP-ribose) polymerase-1 was increased, but that of histone deacetylase 2 was decreased in association with AE-COPD. The expression of modulatory subunit of glutamyl–cysteine ligase was higher and that of its catalytic subunit, together with the expression of dipeptidyl peptidase 4, was lower in COPD patients compared with non-obstructive smokers and non-smokers. Leukotriene A4 hydrolase saw increased expression in patients with COPD according to disease severity compared to non-obstructive individuals, whereas the expression of GSH peroxidase increased in non-obstructive smokers and COPD patients with the growing number of pack-years smoked. The results corroborate COPD and its acute exacerbation as a complex systemic disorder demonstrating distinct associations with the expression of enzymes linked to inflammation and the regulation of GSH metabolism. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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Review

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33 pages, 2687 KB

Open AccessReview

Oxidized Low-Density Lipoprotein as a Potential Target for Enhancing Immune Checkpoint Inhibitor Therapy in Microsatellite-Stable Colorectal Cancer

by Xiaochun Zhang, Xiaorui Ye and Heiying Jin

Antioxidants 2025, 14(6), 726; https://doi.org/10.3390/antiox14060726 - 13 Jun 2025

Cited by 1 | Viewed by 1939

Abstract

Oxidized low-density lipoprotein (oxLDL) exhibits differential expression in microsatellite-stable (MSS) and microsatellite instability-high (MSI) colorectal cancer (CRC), highlighting its potential therapeutic role in immune checkpoint inhibitor (ICI) resistance in MSS CRC. Elevated oxLDL levels in MSS CRC contribute to tumor progression and diminish ICI efficacy by modulating metabolic reprogramming and immunosuppressive mechanisms within the tumor microenvironment (TME) by activating receptors such as LOX-1 and CD36. oxLDL triggers signaling pathways, including NF-κB, PI3K/Akt, and MAPK, leading to the expansion of immunosuppressive cells like regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and M2 macrophages, while concurrently suppressing effector T cell functions. Additionally, oxLDL enhances oxidative stress and promotes fatty acid oxidation (FAO) and glycolytic metabolism, resulting in nutrient competition within the TME and establishing an immunosuppressive milieu, ultimately culminating in ICI resistance. This review systematically examines the disparities in oxLDL expression between MSS and MSI CRC and elucidates the molecular mechanisms through which oxLDL mediates ICI resistance. Furthermore, it explores potential therapeutic strategies targeting oxLDL, offering novel avenues to overcome immunotherapy resistance in MSS CRC. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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21 pages, 948 KB

Open AccessReview

Overview of Oxidative Stress in Systemic Lupus Erythematosus

by Ancuta Lupu, Gabriela Stoleriu, Alin Horatiu Nedelcu, Sara Nadeea Perju, Cristina Gavrilovici, Ginel Baciu, Cristina Maria Mihai, Tatiana Chisnoiu, Ionela Daniela Morariu, Ecaterina Grigore, Shwan Karwan Shawais, Delia Lidia Salaru, Ninel Revenco and Vasile Valeriu Lupu

Antioxidants 2025, 14(3), 303; https://doi.org/10.3390/antiox14030303 - 1 Mar 2025

Cited by 5 | Viewed by 2377

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease that is frequently diagnosed in female patients, caused by multiple interacting factors. It has a complex pathogenesis which can affect almost any organ, from the kidneys to the cardiovascular, pulmonary, neurological, osteoarticular, and hematological systems. The present narrative review seeks to elucidate the role of reactive oxygen species (ROS) in the pathogenesis of SLE. The central question guiding this study is to what extent these serum protein modifications correlate with disease activity and organ damage in SLE. It is characterized by the decreased apoptosis and increased necrosis of T cells and the NETosis of granulocytes. Given the impact of an SLE diagnosis on one’s life, this narrative review aims to evaluate the intricacies of oxidative stress and its relevance to the pathogenesis and treatment of the disease. Topics such as understanding processes of oxidative stress, their damaging pathways, oxidative stress biomarkers, and their role in the future assistance of clinical decisions will be discussed in the article. The accurate determination of biomarkers is taught to improve both the diagnosis and the management of the disease, while antioxidant therapy may open a new door for the treatment. Full article

(This article belongs to the Special Issue Exploring Biomarkers of Oxidative Stress in Health and Disease)

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