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Antioxidants
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Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection—2nd...
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Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection—2nd Edition

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 November 2025 | Viewed by 2110

Special Issue Editors

Dr. Maja Jazvinšćak Jembrek

E-Mail Website
Guest Editor
1. Division of Molecular Medicine, Rudjer Boskovic Institute, 10000 Zagreb, Croatia
2. School of Medicine, Catholic University of Croatia, 10000 Zagreb, Croatia
Interests: neuroprotection; neurotoxicity; neurodegenerative diseases; oxidative stress; polyphenols; neuropharmacology
Special Issues, Collections and Topics in MDPI journals
Dr. Josipa Vlainić

E-Mail Website
Guest Editor
Ruđer Bošković Institute, Division of Molecular Medicine, Laboratory of Molecular Neuropharmacology, POB 180, Zagreb, Croatia
Interests: pharmacology; neuroscience; natural products; antioxidant capacity; antimicrobial potential
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Building on the success of our previous edition, which focused on the neuroprotective strategies targeting oxidative stress and related signaling pathways, we are pleased to announce the second edition of the Special Issue entitled “Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection”. This edition expands our scope to include the prooxidative mechanisms of compounds traditionally classified as antioxidants, exploring both their neuroprotective and potential neurotoxic effects.

Oxidative stress is recognized as a key driver of neuronal injury and dysfunction in many neurological diseases. While extensive research has advanced our understanding of redox imbalance and redox-sensitive signaling pathways in neuroprotection, substantial gaps remain in identifying the factors that modulate neuronal responses to specific compounds under oxidative conditions. Compounds of natural and synthetic origin, appreciated for their ability to restore redox balance and attenuate oxidative stress in injured cells, can, under certain conditions (such as metal dyshomeostasis), exhibit prooxidative behaviors.

Studies that shed light on the factors and intracellular signaling pathways that govern whether these agents act in an antioxidative or prooxidative manner, impacting cell survival or death, are particularly welcome. A better characterization of the cellular and molecular mechanisms involved, as well as any off-target effects that may drive specific antioxidative or prooxidative outcomes, could help to bridge any critical gaps in our understanding. Such insights are essential for guiding the development of more effective therapies for neurological disorders, a long-awaited advancement in the field.

We look forward to your contributions to this Special Issue!

Dr. Maja Jazvinšćak Jembrek
Dr. Josipa Vlainić
Guest Editors

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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • neuroprotection
  • neurotoxicity
  • antioxidative vs. proxidative
  • oxidative stress
  • signaling pathways
  • redox metals

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Published Papers (2 papers)

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19 pages, 8260 KiB  
Article
Peptide Fraction from Naja mandalayensis Snake Venom Showed Neuroprotection Against Oxidative Stress in Hippocampal mHippoE-18 Cells but Not in Neuronal PC12 Cells
by Brenda R. Silva, Lais C. Mendes, Marcela B. Echeverry, Maria Aparecida Juliano, Emidio Beraldo-Neto and Carlos Alberto-Silva
Antioxidants 2025, 14(3), 277; https://doi.org/10.3390/antiox14030277 - 26 Feb 2025
Viewed by 654
Abstract
Functional characterization of peptide fraction (PF) from snake venom has provided novel opportunities to investigate possible neuroprotective compounds relevant to pharmaceuticals. This study was performed to investigate the PF-mediated neuroprotection obtained from Naja mandalayensis snake venom, a member of the Elapidae family, using [...] Read more.
Functional characterization of peptide fraction (PF) from snake venom has provided novel opportunities to investigate possible neuroprotective compounds relevant to pharmaceuticals. This study was performed to investigate the PF-mediated neuroprotection obtained from Naja mandalayensis snake venom, a member of the Elapidae family, using two neuronal cell lines, undifferentiated PC12 and differentiated mHippoE-18, in response to H2O2-induced oxidative stress. Cells were pre-treated for 4 h with PF (10, 1, 0.01, and 0.001 μg mL−1), and thereafter exposed to H2O2 (0.5 mmol L−1) for 20 h. Then, the oxidative stress markers and label-free differential proteome strategy were analyzed to understand the neuroprotective effects of PF. In PC12 cells, PF showed no neuroprotective effects against oxidative stress. In mHippoE-18 cells, PF at 0.01 and 0.001 μg mL−1 increased the viability and metabolism of cells against H2O2-induced neurotoxicity, reducing reactive oxygen species (ROS) generation. Interestingly, PF also exhibited a substantial reduction in baseline ROS levels compared to the control, indicating that PF could have compounds with antioxidant features. The comparative proteomic profiling identified 53 proteins with differential expression related to antioxidant action, catalysis, molecular function regulators, structural molecule activity, translation regulatory activity, ATP, and binding. The PF + H2O2 group indicated that protein expression is 6% upregulated, 4% downregulated, and 94% unchanged compared to the H2O2 group. Three significant proteins upregulated in the PF + H2O2 group, including elongation factor 2 (P58252), proteasome subunit alpha type (E9Q0X0), and E2 ubiquitin-conjugating enzyme (A0A338P786), suggested that PF-mediated neuroprotection happens through translational regulation and the degradation of defective proteins via the proteasome complex. Additionally, differential protein expression in PF changed the metabolism, protein synthesis, synaptic activity, and intracellular transport, suggesting that PF contains the rich mixture of bioactive peptides of interest pharmacologically. Overall, this study offers new opportunities for evaluating whether PF’s neuroprotective features in specific neuronal cells are maintained and to investigate neurodegenerative disease drug development processes. Full article
(This article belongs to the Special Issue Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection—2nd Edition)
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29 pages, 5402 KiB  
Article
Neurotoxic Effect of Myricitrin in Copper-Induced Oxidative Stress Is Mediated by Increased Intracellular Ca2+ Levels and ROS/p53/p38 Axis
by Ignacija Vlašić, Antonio Krstačić-Galić, Anđela Horvat, Nada Oršolić, Anja Sadžak, Lucija Mandić, Suzana Šegota and Maja Jazvinšćak Jembrek
Antioxidants 2025, 14(1), 46; https://doi.org/10.3390/antiox14010046 - 3 Jan 2025
Viewed by 1021
Abstract
Although commonly appreciated for their anti-oxidative and neuroprotective properties, flavonoids can also exhibit pro-oxidative activity, potentially reducing cell survival, particularly in the presence of metal ions. Disrupted copper homeostasis is a known contributor to neuronal dysfunction through oxidative stress induction. This study investigated [...] Read more.
Although commonly appreciated for their anti-oxidative and neuroprotective properties, flavonoids can also exhibit pro-oxidative activity, potentially reducing cell survival, particularly in the presence of metal ions. Disrupted copper homeostasis is a known contributor to neuronal dysfunction through oxidative stress induction. This study investigated the effects of myricitrin (1–20 μg/mL) on copper-induced toxicity (0.5 mM CuSO4) in the neuroblastoma SH-SY5Y cell line. At non-toxic concentrations, myricitrin exacerbated copper’s toxic effects. The myricitrin-induced decrease in survival was accompanied with increased reactive oxygen species (ROS) production, reduced superoxide dismutase activity, and a lower GSH/GSSG ratio. In combination with copper, myricitrin also activated caspase-3/7, promoted nuclear chromatin changes, and compromised membrane integrity. At the protein level, myricitrin upregulated p53 and PUMA expression. The toxic effects of myricitrin were alleviated by the p38 inhibitor SB203580, the intracellular calcium chelator BAPTA-AM, and the NMDA receptor blocker MK-801, highlighting the significant role of the ROS/p53/p38 axis in cell death and the critical involvement of calcium ions in apoptosis induction. The atomic force microscopy was used to assess the surface morphology and nanomechanical properties of SH-SY5Y cells, revealing changes following myricitrin treatment. This research highlights the toxic potential of myricitrin and emphasizes the need for caution when considering flavonoid supplementation in conditions with elevated copper levels. Full article
(This article belongs to the Special Issue Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection—2nd Edition)
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