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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: 25 November 2025 | Viewed by 424

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Department of Veterinary Sciences, University of Messina, Via Palatucci Annunziata, 98168 Messina, Italy
Interests: biochemistry; veterinary medicine; molecular biology
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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

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Keywords

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

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Published Papers (1 paper)

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Research

21 pages, 7342 KiB  
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
Viewed by 291
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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