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Oxidative Stress and Disease: Basic and Biochemical Approaches
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Oxidative Stress and Disease: Basic and Biochemical Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 28 February 2027 | Viewed by 5021

Editor

Dr. Giuseppe Bruschetta

E-Mail Website
Guest Editor
Department of Veterinary Sciences, University of Messina, Via Palatucci Annunziata, 98168 Messina, Italy
Interests: biochemistry; veterinary medicine; molecular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pollution, smoking, excessive alcohol consumption, and stress (external factors), in addition to metabolic processes in cells, such as respiration and digestion, produce many reactive oxygen species (ROS) and nitrogen species every day. These unstable molecules cause oxidative stress, an imbalance between ROS and nitrogen species in the cell, and affect its ability to neutralize them. Oxidative stress has detrimental effects, such as the onset of inflammatory processes and/or causing damage to cellular proteins, lipids, and nucleic acids. These negative effects must be counteracted by antioxidant biochemical pathways.

Moreover, oxidative stress is implicated in the development of diseases, including cancer, and many studies have investigated the use of antioxidants for the prevention and treatment of cardiovascular diseases and neurodegenerative disorders.

The determination of lipid peroxidation (MDA) and enzymes, such as catalase (CAT), superoxide dismutase (SOD), myeloperoxidase (MPO), and butyrylcholinesterase (BuChe), can provide information on the degree of oxidative stress. Furthermore, cytokines’ and prostaglandins’ monitoring provides a measure of the inflammatory state.

The molecular evaluation of inflammatory oxidative stress may represent a useful biochemical approach for comparing different drug administrations for various pathologies. Therefore, this Special Issue encourages manuscript submissions on oxidative stress, its biochemical pathways, and potential interventions to mitigate its harmful effects.

Dr. Giuseppe Bruschetta
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • aging
  • antioxidant mechanisms
  • cancer
  • cytokines
  • enzymatic pathways
  • inflammatory processes
  • oxidative stress
  • reactive oxygen species (ROS)

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Published Papers (3 papers)

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Research

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18 pages, 2230 KB  
Article
Serum Copper-to-Zinc Ratio and Oxidative Stress Are Associated with Anemia in Older Adults with Cardiovascular–Kidney–Metabolic Syndrome
by Giuseppe Bruschetta, Guido Gembillo, Lorenzo Lo Cicero, Angela D’Ascola, Fabio Bruno, Andrea Corsonello, Domenico Santoro, Mirko Di Rosa and Luca Soraci
Int. J. Mol. Sci. 2026, 27(13), 5840; https://doi.org/10.3390/ijms27135840 - 28 Jun 2026
Cited by 2 | Viewed by 617
Abstract
Chronic oxidative stress is a molecular hallmark of cardiovascular–kidney–metabolic (CKM) syndrome, yet its contribution to CKM-associated anemia beyond erythropoietin deficiency and iron restriction is poorly characterized. The serum copper-to-zinc (Cu/Zn) ratio reflects impaired Cu/Zn-SOD1 antioxidant capacity and inflammatory trace-element imbalance, but its relationships [...] Read more.
Chronic oxidative stress is a molecular hallmark of cardiovascular–kidney–metabolic (CKM) syndrome, yet its contribution to CKM-associated anemia beyond erythropoietin deficiency and iron restriction is poorly characterized. The serum copper-to-zinc (Cu/Zn) ratio reflects impaired Cu/Zn-SOD1 antioxidant capacity and inflammatory trace-element imbalance, but its relationships with circulating redox biomarkers and its hematological relevance in CKM syndrome has never been explored in a community-dwelling cohort of older adults. We analyzed 2391 NHANES 2011–2016 participants ≥ 50 years of age with CKM stage I-IV. To explore whether the serum Cu/Zn ratio was associated with oxidative stress and immunomodulatory biomarkers as well as with the odds of anemia, we used survey-weighted Spearman correlations, linear regression (outcome: hemoglobin), and logistic regression (outcome: anemia); multivariate models were adjusted for a panel of antioxidant or immunomodulatory biomarkers (selenium, vitamin D), pro-oxidant biomarkers (lead, cadmium, cotinine, uric acid), red cell distribution width (RDW) as a composite biomarker of erythrocyte stress, neutrophil-to-lymphocyte ratio (NLR), CKM stage, and comorbidities. The molecular targets of the nine biomarkers were mapped onto a protein–protein interaction network using the STRING database v12.0 to contextualize regression findings within a systems biology framework. Anemia was present in 205 participants (8.6%). The Cu/Zn ratio was inversely correlated with the antioxidant marker selenium (r = −0.19; p < 0.001) and positively correlated with the pro-oxidant markers RDW (r = +0.21; p < 0.001) and cadmium (r = +0.10; p < 0.001), consistent with its role as a hub within the CKM redox network. In fully adjusted models, a higher Cu/Zn ratio was independently associated with prevalent anemia (OR = 2.94; 95% CI: 1.61–5.37) and lower hemoglobin (β = −0.55 g/dL); among included biomarkers, selenium and cadmium were independently protective (OR = 0.76 per 10 µg/L and 0.23 per µg/dL, respectively), and RDW and uric acid were independently harmful (OR = 2.20 per 1% and 1.33 per mg/dL, respectively). The Cu/Zn ratio correlated with both antioxidant depletion and pro-oxidant accumulation in CKM syndrome and was independently associated with anemia within this oxidative network. Together with selenium, cadmium, RDW, and uric acid, it defines an oxidative stress-driven hematological pathway that may contribute to the development and progression of anemia in patients with CKM syndrome. Full article
(This article belongs to the Special Issue Oxidative Stress and Disease: Basic and Biochemical Approaches)
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21 pages, 7342 KB  
Article
Synergistic Antioxidant Effects of C3G-Enriched Oryza sativa L. cv. RD83 Extract and α-Tocopherol Against H2O2-Induced Oxidative Stress in SH-SY5Y Cells
by Nootchanat Mairuae and Nut Palachai
Int. J. Mol. Sci. 2025, 26(13), 6490; https://doi.org/10.3390/ijms26136490 - 5 Jul 2025
Cited by 5 | Viewed by 1507
Abstract
Oxidative stress, which contributes to neuronal cell dysfunction, is a critical factor in the pathogenesis of neurodegenerative diseases. Anthocyanins and α-tocopherol have shown potential in mitigating oxidative damage, and their combination may provide synergistic effects. This study investigated the combined effects of a [...] Read more.
Oxidative stress, which contributes to neuronal cell dysfunction, is a critical factor in the pathogenesis of neurodegenerative diseases. Anthocyanins and α-tocopherol have shown potential in mitigating oxidative damage, and their combination may provide synergistic effects. This study investigated the combined effects of a cyanidin-3-glucoside (C3G)-enriched extract derived from Oryza sativa L. cv. RD83 and α-tocopherol (C3GE) on hydrogen peroxide (H2O2)-induced oxidative stress in SH-SY5Y cells. Cells were treated with C3GE during exposure to 200 µM H2O2. Cell viability, intracellular reactive oxygen species (ROS), and oxidative stress biomarkers, including the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), as well as malondialdehyde (MDA) levels, were evaluated. Protein expression levels of histone deacetylase 1 (HDAC1), nuclear factor erythroid 2 related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and SOD1 were also assessed. The combined treatment markedly improved cell viability, suppressed ROS accumulation, enhanced antioxidant enzyme activities, and significantly reduced MDA levels, suggesting effective protection against oxidative damage. Mechanistically, C3GE downregulated HDAC1 expression while upregulating Nrf2, HO-1, and SOD1, indicating that its antioxidant and neuroprotective effects are mediated, at least in part, through epigenetic modulation of redox-related signaling pathways. These results demonstrate a synergistic interaction between C3G and α-tocopherol that enhances cellular antioxidant defenses and supports redox homeostasis. In conclusion, the C3GE combination offers a promising therapeutic approach for preventing or attenuating oxidative stress-induced neuronal injury, with potential relevance for the treatment of neurodegenerative disorders. Full article
(This article belongs to the Special Issue Oxidative Stress and Disease: Basic and Biochemical Approaches)
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Review

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37 pages, 4999 KB  
Review
Oxidative Stress Biomarkers in Oral Mucosal Wound Healing and Photobiomodulation: Biochemical Pathways, Experimental Models, and Translational Perspectives
by Ilija M. Dragojević, Bojana Kisić, Dijana Mirić, Aleksandra Ilić, Jelena T. Todić, Milena Kostić, Zlatibor Anđelković, Ljiljana Popović, Ljiljana Šubarić, Aleksandar Šubarić and Nadica S. Đorđević
Int. J. Mol. Sci. 2026, 27(13), 5763; https://doi.org/10.3390/ijms27135763 - 26 Jun 2026
Viewed by 603
Abstract
Oral mucosal repair is a redox-regulated process that may be impaired by diabetes, chronic inflammation, infection, and chemotherapy- or radiotherapy-induced oral mucositis. Reactive oxygen species (ROS) support host defense, epithelial migration, angiogenesis, extracellular matrix remodeling, and adaptive repair when their production is transient [...] Read more.
Oral mucosal repair is a redox-regulated process that may be impaired by diabetes, chronic inflammation, infection, and chemotherapy- or radiotherapy-induced oral mucositis. Reactive oxygen species (ROS) support host defense, epithelial migration, angiogenesis, extracellular matrix remodeling, and adaptive repair when their production is transient and compartmentalized. In contrast, persistent ROS promote lipid, protein, and DNA oxidation, mitochondrial dysfunction, and extracellular matrix damage. Photobiomodulation (PBM) is increasingly used to support oral tissue repair, but its effects should be interpreted as dose- and context-dependent redox modulation rather than as simple antioxidant activity. This narrative review synthesizes oxidative stress biomarkers and redox-sensitive pathways relevant to oral mucosal repair and PBM, including oxidant–antioxidant balance, lipid and protein oxidation, oxidative DNA damage, antioxidant defense, thiol/disulfide homeostasis, mitochondrial and NADPH oxidase-derived ROS, Nrf2/HO-1, NF-κB, HIF-1α/VEGF, MAPK/ERK, PI3K/Akt, and MMP/TIMP signaling. The review emphasizes the distinction between transient mitochondrial ROS/nitric oxide signaling and sustained NADPH oxidase-driven oxi-inflammatory stress. It proposes a practical redox-guided framework for biomarker selection, PBM response interpretation, and future study design, while noting that this framework remains conceptual and is not yet a validated clinical decision algorithm. Full article
(This article belongs to the Special Issue Oxidative Stress and Disease: Basic and Biochemical Approaches)
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