Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.6
6.0
Journals
Antioxidants
Special Issues
Role of Super Oxide Dismutase (SOD)1 Isoenzyme and Reactive Oxygen...
share announcement

Role of Super Oxide Dismutase (SOD)1 Isoenzyme and Reactive Oxygen Species (ROS) Generation in Cellular 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: closed (30 September 2024) | Viewed by 5465

Special Issue Editors

Prof. Paolo Mondola

E-Mail Website
Guest Editor
Section of Human Physiology, Department of Medicina Clinica e Chirurgia, University of Naples “Federico II”, Naples, Italy
Interests: SOD-1; signal transduction; muscarinic receptors; cell secretion; cell physiology
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppina Ruggiero

E-Mail Website
Guest Editor
Dipartimento di Scienze Mediche Traslazionali, Università di Napoli “Federico II”, 80131 Naples, Italy
Interests: adaptive immunity; immune mediated diseases; SOD-1; immune regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Intracellular Reactive Oxygen Species (ROS) have been recognised as key second messengers for a series of receptor/ligand interactions. Moreover, ROS involvement in the regulation of neuronal networks as well as of antigen-dependent T cell responses has been largely demonstrated.

ROS-dependent regulatory networks are usually mediated by peroxides. SOD enzymes physiologically mediate the scavenging of ROS to H2O2 and molecular oxygen. Particularly, SOD1 has been observed to interfere with multiple intracellular signalling networks, independently from its enzymatic activity. Indeed, SOD1/M1 muscarinic receptor interaction has been shown to mediate the activation of Protein Kinase C (PKC)-dependent signalling pathways and increase in intracellular Ca++ level in excitable cells. Moreover, mTOR enzyme, a key molecule for differentiation of the Treg immune-modulating subset, has been described to regulate SOD1 activity.

A series of physiological inputs have been observed to mediate SOD-1 exocytosis, thus inducing increased interaction of the enzyme with a complex molecular network involved in the regulation of multiple biological processes. These findings add SOD to the molecules to be potentially targeted for innovative therapeutic approaches.

We invite you to submit your latest research findings or review/perspective articles to this Special Issue, which plans to bring together current research concerning SOD-dependent pathways in both physiological and pathological processes. We will welcome in vitro and in vivo studies related to SOD structure/function; the regulation of SOD production, intracellular localization and extracellular export; SOD posttranslational modifications; and the role of SOD in cell signalling, cell metabolism, cell cycle regulation, epigenetic pathway modulation, cellular stress managing and disease pathogenesis.

We look forward to your contribution.

Prof. Paolo Mondola
Dr. Giuseppina Ruggiero
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

  • superoxide dismutase (SOD) isoenzymes
  • superoxide dismutase (SOD)1
  • cell signalling
  • cell metabolism
  • cell functions
  • cellular stress
  • disease pathogenesis

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

20 pages, 4428 KiB  
Article
SOD1 Is an Integral Yet Insufficient Oxidizer of Hydrogen Sulfide in Trisomy 21 B Lymphocytes and Can Be Augmented by a Pleiotropic Carbon Nanozyme
by Karthik Mouli, Anton V. Liopo, Larry J. Suva, Kenneth R. Olson, Emily A. McHugh, James M. Tour, Paul J. Derry and Thomas A. Kent
Antioxidants 2024, 13(11), 1361; https://doi.org/10.3390/antiox13111361 - 7 Nov 2024
Cited by 2 | Viewed by 2348
Abstract
Down syndrome (DS) is a multisystemic disorder that includes accelerated aging caused by trisomy 21. In particular, overexpression of cystathionine-β-synthase (CBS) is linked to excess intracellular hydrogen sulfide (H2S), a mitochondrial toxin at higher concentrations, which impairs cellular viability. Concurrent overexpression [...] Read more.
Down syndrome (DS) is a multisystemic disorder that includes accelerated aging caused by trisomy 21. In particular, overexpression of cystathionine-β-synthase (CBS) is linked to excess intracellular hydrogen sulfide (H2S), a mitochondrial toxin at higher concentrations, which impairs cellular viability. Concurrent overexpression of superoxide dismutase 1 (SOD1) may increase oxidative stress by generating excess hydrogen peroxide (H2O2) while also mitigating the toxic H2S burden via a non-canonical sulfide-oxidizing mechanism. We investigated the phenotypic variability in basal H2S levels in relation to DS B lymphocyte cell health and SOD1 in H2S detoxification. The H2S levels were negatively correlated with the DS B lymphocyte growth rates but not with CBS protein. Pharmacological inhibition of SOD1 using LCS-1 significantly increased the H2S levels to a greater extent in DS cells while also decreasing the polysulfide products of H2S oxidation. However, DS cells exhibited elevated H2O2 and lipid peroxidation, representing potential toxic consequences of SOD1 overexpression. Treatment of DS cells with a pleiotropic carbon nanozyme (pleozymes) decreased the total oxidative stress and reduced the levels of the H2S-generating enzymes CBS and 3-mercaptopyruvate sulfurtransferase (MPST). Our results indicate that pleozymes may bridge the protective and deleterious effects of DS SOD1 overexpression on H2S metabolism and oxidative stress, respectively, with cytoprotective benefits. Full article
(This article belongs to the Special Issue Role of Super Oxide Dismutase (SOD)1 Isoenzyme and Reactive Oxygen Species (ROS) Generation in Cellular Pathophysiology)
►▼ Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1180 KiB  
Review
Insights on the Multifaceted Roles of Wild-Type and Mutated Superoxide Dismutase 1 in Amyotrophic Lateral Sclerosis Pathogenesis
by Valentina Rubino, Giuliana La Rosa, Luca Pipicelli, Flavia Carriero, Simona Damiano, Mariarosaria Santillo, Giuseppe Terrazzano, Giuseppina Ruggiero and Paolo Mondola
Antioxidants 2023, 12(9), 1747; https://doi.org/10.3390/antiox12091747 - 10 Sep 2023
Cited by 3 | Viewed by 2351
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a progressive motor neurodegenerative disease. Cell damage in ALS is the result of many different, largely unknown, pathogenetic mechanisms. Astrocytes and microglial cells play a critical role also for their ability to enhance a deranged inflammatory response. Excitotoxicity, [...] Read more.
Amyotrophic Lateral Sclerosis (ALS) is a progressive motor neurodegenerative disease. Cell damage in ALS is the result of many different, largely unknown, pathogenetic mechanisms. Astrocytes and microglial cells play a critical role also for their ability to enhance a deranged inflammatory response. Excitotoxicity, due to excessive glutamate levels and increased intracellular Ca2+ concentration, has also been proposed to play a key role in ALS pathogenesis/progression. Reactive Oxygen Species (ROS) behave as key second messengers for multiple receptor/ligand interactions. ROS-dependent regulatory networks are usually mediated by peroxides. Superoxide Dismutase 1 (SOD1) physiologically mediates intracellular peroxide generation. About 10% of ALS subjects show a familial disease associated with different gain-of-function SOD1 mutations. The occurrence of sporadic ALS, not clearly associated with SOD1 defects, has been also described. SOD1-dependent pathways have been involved in neuron functional network as well as in immune-response regulation. Both, neuron depolarization and antigen-dependent T-cell activation mediate SOD1 exocytosis, inducing increased interaction of the enzyme with a complex molecular network involved in the regulation of neuron functional activity and immune response. Here, alteration of SOD1-dependent pathways mediating increased intracellular Ca2+ levels, altered mitochondria functions and defective inflammatory process regulation have been proposed to be relevant for ALS pathogenesis/progression. Full article
(This article belongs to the Special Issue Role of Super Oxide Dismutase (SOD)1 Isoenzyme and Reactive Oxygen Species (ROS) Generation in Cellular Pathophysiology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop