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Antioxidants
Special Issues
SOD-1 and Antioxidant Role in Cellular Pathophysiology
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SOD-1 and Antioxidant Role in Cellular Pathophysiology

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 4721

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
Department of Scienze Mediche Traslazionali, University of Naples “Federico II”, Naples, Italy
Interests: adaptive immunity; immune mediated diseases; SOD-1; immune regulation

Special Issue Information

Dear Colleagues,

Cellular metabolism continuously produces several types of reactive oxygen species (ROS), mainly superoxide anion, hydrogen peroxide, and their reactive products. Superoxide dismutase (SODs) isoenzymes help in the dismutation of the high reactive and instable oxygen radical in molecular oxygen and more stable hydrogen peroxide. Oxygen metabolites have been largely demonstrated to be involved in maintaining cellular homeostasis by playing a role in regulating physiological cell metabolism and finely tuning cell signaling in a variety of cell types.

It has been demonstrated that among the SOD family, the cytosolic dimeric CuZn superoxide dismutase molecule (SOD-1) might interfere with intracellular signaling network independently from its enzymatic activity; in addition, both hydrogen peroxide and SOD-1-dependent regulatory pathways have been described in different cell types in human and mouse models.

The involvement of SOD-1-dependent molecular networks in the pathogenesis of different human diseases such as cancer, neurodegeneration, ischemia/reperfusion injuries, and immune-mediated conditions has been convincingly described. These findings add SOD-1 to the molecules to be potentially targeted in innovative therapeutic approaches.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning SOD-1 involvement in both physiological processes as well as diseased states. This research can include both in vitro and in vivo studies relating to any of the following topics: structure/function of SOD-1; regulation of SOD-1 production, intracellular localization, and extracellular export; posttranslational modifications of SOD-1; role of SOD-1 in cell signaling, cell metabolism, cell cycle regulation, epigenetic pathway modulation, cellular stress managing, and disease pathogenesis.

We look forward to your contribution.

Dr. 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)-1
  • Cell signaling
  • Cell metabolism
  • Cell functions
  • Cellular stress
  • Disease pathogenesis

Published Papers (2 papers)

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9 pages, 1961 KiB  
Article
Caudal–Rostral Progression of Alpha Motoneuron Degeneration in the SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis
by Alastair J. Kirby, Thomas Palmer, Richard J. Mead, Ronaldo M. Ichiyama and Samit Chakrabarty
Antioxidants 2022, 11(5), 983; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050983 - 17 May 2022
Cited by 3 | Viewed by 1614
Abstract
Mice with transgenic expression of human SOD1G93A are a widely used model of ALS, with a caudal–rostral progression of motor impairment. Previous studies have quantified the progression of motoneuron (MN) degeneration based on size, even though alpha (α-) and gamma (γ-) MNs [...] Read more.
Mice with transgenic expression of human SOD1G93A are a widely used model of ALS, with a caudal–rostral progression of motor impairment. Previous studies have quantified the progression of motoneuron (MN) degeneration based on size, even though alpha (α-) and gamma (γ-) MNs overlap in size. Therefore, using molecular markers and synaptic inputs, we quantified the survival of α-MNs and γ-MNs at the lumbar and cervical spinal segments of 3- and 4-month SOD1G93A mice, to investigate whether there is a caudal–rostral progression of MN death. By 3 months, in the cervical and lumbar spinal cord, there was α-MN degeneration with complete γ-MN sparing. At 3 months, the cervical spinal cord had more α-MNs per ventral horn than the lumbar spinal cord in SOD1G93A mice. A similar spatial trend of degeneration was observed in the corticospinal tract, which remained intact in the cervical spinal cord at 3- and 4- months of age. These findings agree with the corticofugal synaptopathy model that α-MNs and CST of the lumbar spinal cord are more susceptible to degeneration in SOD1G93A mice. Hence, there is a spatial and temporal caudal–rostral progression of α-MN and CST degeneration in SOD1G93A mice. Full article
(This article belongs to the Special Issue SOD-1 and Antioxidant Role in Cellular Pathophysiology)
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15 pages, 731 KiB  
Article
Superoxide Dismutase-1 Intracellular Content in T Lymphocytes Associates with Increased Regulatory T Cell Level in Multiple Sclerosis Subjects Undergoing Immune-Modulating Treatment
by Valentina Rubino, Anna Teresa Palatucci, Giuliana La Rosa, Angela Giovazzino, Francesco Aruta, Simona Damiano, Flavia Carriero, Mariarosaria Santillo, Rosa Iodice, Paolo Mondola, Giuseppina Ruggiero and Giuseppe Terrazzano
Antioxidants 2021, 10(12), 1940; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121940 - 03 Dec 2021
Cited by 4 | Viewed by 2345
Abstract
Reactive oxygen species (ROS) participate in the T-cell activation processes. ROS-dependent regulatory networks are usually mediated by peroxides, which are more stable and able to freely migrate inside cells. Superoxide dismutase (SOD)-1 represents the major physiological intracellular source of peroxides. We found that [...] Read more.
Reactive oxygen species (ROS) participate in the T-cell activation processes. ROS-dependent regulatory networks are usually mediated by peroxides, which are more stable and able to freely migrate inside cells. Superoxide dismutase (SOD)-1 represents the major physiological intracellular source of peroxides. We found that antigen-dependent activation represents a triggering element for SOD-1 production and secretion by human T lymphocytes. A deranged T-cell proinflammatory response characterizes the pathogenesis of multiple sclerosis (MS). We previously observed a decreased SOD-1 intracellular content in leukocytes of MS individuals at diagnosis, with increasing amounts of such enzyme after interferon (IFN)-b 1b treatment. Here, we analyzed in depth SOD-1 intracellular content in T cells in a cohort of MS individuals undergoing immune-modulating treatment. Higher amounts of the enzyme were associated with increased availability of regulatory T cells (Treg) preferentially expressing Foxp3-exon 2 (Foxp3-E2), as described for effective Treg. In vitro administration of recombinant human SOD-1 to activated T cells, significantly increased their IL-17 production, while SOD-1 molecules lacking dismutase activity were unable to interfere with cytokine production by activated T cells in vitro. Furthermore, hydrogen peroxide addition was observed to mimic, in vitro, the SOD-1 effect on IL-17 production. These data add SOD-1 to the molecules involved in the molecular pathways contributing to re-shaping the T-cell cytokine profile and Treg differentiation. Full article
(This article belongs to the Special Issue SOD-1 and Antioxidant Role in Cellular Pathophysiology)
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