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Oxidative Eustress and Distress: Mitochondrial Reactive Oxygen Species in Health...
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Oxidative Eustress and Distress: Mitochondrial Reactive Oxygen Species in Health and Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6609

Special Issue Editor

Dr. Ryan Mailloux

E-Mail Website
Guest Editor
School of Human Nutrition, Faculty of Agricultural and Environmental Sciences, McGill University, Montreal, QC, Canada
Interests: mitochondria; bioenergetics; redox homeostasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are called the “powerhouses of the cell” for a good reason. Mitochondria use redox reactions to extract electrons from nutrients to produce large quantities of ATP, the universal energy currency. Electron transfer reactions in mitochondria are not perfectly coupled to ATP production. At various points in several metabolic and electron transferring pathways, electrons can spin off and prematurely react with molecular oxygen (O2) to generate reactive oxygen species (ROS). These “by-products” of ATP production can be toxic in large quantities, induce oxidative stress and cell damage. Lower quantities, however, can be beneficial and are involved in many signaling pathways. This dichotomy has led to the development of new terms that extend off the original definition for oxidative stress to account for the positive and negative effects of ROS. These terms are oxidative “eustress”, for a positive oxidative event, versus “distress”, which can be toxic. The present Special Issue focuses on mitochondrial bioenergetics in eustress signaling and distress and their roles in health and disease.

Dr. Ryan Mailloux
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 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • ROS
  • redox signaling
  • oxidative stress
  • mitochondria
  • bioenergetics

Published Papers (3 papers)

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Research

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13 pages, 3913 KiB  
Article
Myelin Disruption, Neuroinflammation, and Oxidative Stress Induced by Sulfite in the Striatum of Rats Are Mitigated by the pan-PPAR agonist Bezafibrate
by Nícolas Manzke Glänzel, Belisa Parmeggiani, Mateus Grings, Bianca Seminotti, Morgana Brondani, Larissa D. Bobermin, César A. J. Ribeiro, André Quincozes-Santos, Jerry Vockley and Guilhian Leipnitz
Cells 2023, 12(12), 1557; https://doi.org/10.3390/cells12121557 - 6 Jun 2023
Cited by 1 | Viewed by 1542
Abstract
Sulfite predominantly accumulates in the brain of patients with isolated sulfite oxidase (ISOD) and molybdenum cofactor (MoCD) deficiencies. Patients present with severe neurological symptoms and basal ganglia alterations, the pathophysiology of which is not fully established. Therapies are ineffective. To elucidate the pathomechanisms [...] Read more.
Sulfite predominantly accumulates in the brain of patients with isolated sulfite oxidase (ISOD) and molybdenum cofactor (MoCD) deficiencies. Patients present with severe neurological symptoms and basal ganglia alterations, the pathophysiology of which is not fully established. Therapies are ineffective. To elucidate the pathomechanisms of ISOD and MoCD, we investigated the effects of intrastriatal administration of sulfite on myelin structure, neuroinflammation, and oxidative stress in rat striatum. Sulfite administration decreased FluoromyelinTM and myelin basic protein staining, suggesting myelin abnormalities. Sulfite also increased the staining of NG2, a protein marker of oligodendrocyte progenitor cells. In line with this, sulfite also reduced the viability of MO3.13 cells, which express oligodendroglial markers. Furthermore, sulfite altered the expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1), indicating neuroinflammation and redox homeostasis disturbances. Iba1 staining, another marker of neuroinflammation, was also increased by sulfite. These data suggest that myelin changes and neuroinflammation induced by sulfite contribute to the pathophysiology of ISOD and MoCD. Notably, post-treatment with bezafibrate (BEZ), a pan-PPAR agonist, mitigated alterations in myelin markers and Iba1 staining, and IL-1β, IL-6, iNOS and HO-1 expression in the striatum. MO3.13 cell viability decrease was further prevented. Moreover, pre-treatment with BEZ also attenuated some effects. These findings show the modulation of PPAR as a potential opportunity for therapeutic intervention in these disorders. Full article
(This article belongs to the Special Issue Oxidative Eustress and Distress: Mitochondrial Reactive Oxygen Species in Health and Disease)
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17 pages, 2448 KiB  
Article
Proliferating Astrocytes in Primary Culture Do Not Depend upon Mitochondrial Respiratory Complex I Activity or Oxidative Phosphorylation
by Ellen A. Silva, Ana P. Dalla Costa, Juliana S. Ruas, Edilene S. Siqueira-Santos, Annelise Francisco and Roger F. Castilho
Cells 2023, 12(5), 683; https://doi.org/10.3390/cells12050683 - 21 Feb 2023
Cited by 2 | Viewed by 2145
Abstract
Understanding the role of astrocytes in the development of the nervous system and neurodegenerative disorders implies a necessary knowledge of the oxidative metabolism of proliferating astrocytes. The electron flux through mitochondrial respiratory complexes and oxidative phosphorylation may impact the growth and viability of [...] Read more.
Understanding the role of astrocytes in the development of the nervous system and neurodegenerative disorders implies a necessary knowledge of the oxidative metabolism of proliferating astrocytes. The electron flux through mitochondrial respiratory complexes and oxidative phosphorylation may impact the growth and viability of these astrocytes. Here, we aimed at assessing to which extent mitochondrial oxidative metabolism is required for astrocyte survival and proliferation. Primary astrocytes from the neonatal mouse cortex were cultured in a physiologically relevant medium with the addition of piericidin A or oligomycin at concentrations that fully inhibit complex I-linked respiration and ATP synthase, respectively. The presence of these mitochondrial inhibitors for up to 6 days in a culture medium elicited only minor effects on astrocyte growth. Moreover, neither the morphology nor the proportion of glial fibrillary acidic protein-positive astrocytes in culture was affected by piericidin A or oligomycin. Metabolic characterization of the astrocytes showed a relevant glycolytic metabolism under basal conditions, despite functional oxidative phosphorylation and large spare respiratory capacity. Our data suggest that astrocytes in primary culture can sustainably proliferate when their energy metabolism relies only on aerobic glycolysis since their growth and survival do not require electron flux through respiratory complex I or oxidative phosphorylation. Full article
(This article belongs to the Special Issue Oxidative Eustress and Distress: Mitochondrial Reactive Oxygen Species in Health and Disease)
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Review

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17 pages, 4808 KiB  
Review
Regulation of Mitochondrial Hydrogen Peroxide Availability by Protein S-glutathionylation
by Ryan J. Mailloux, Cathryn Grayson and Olivia Koufos
Cells 2023, 12(1), 107; https://doi.org/10.3390/cells12010107 - 27 Dec 2022
Cited by 13 | Viewed by 2262
Abstract
Background: It has been four decades since protein S-glutathionylation was proposed to serve as a regulator of cell metabolism. Since then, this redox-sensitive covalent modification has been identified as a cell-wide signaling platform required for embryonic development and regulation of many physiological functions. [...] Read more.
Background: It has been four decades since protein S-glutathionylation was proposed to serve as a regulator of cell metabolism. Since then, this redox-sensitive covalent modification has been identified as a cell-wide signaling platform required for embryonic development and regulation of many physiological functions. Scope of the Review: Mitochondria use hydrogen peroxide (H2O2) as a second messenger, but its availability must be controlled to prevent oxidative distress and promote changes in cell behavior in response to stimuli. Experimental data favor the function of protein S-glutathionylation as a feedback loop for the inhibition of mitochondrial H2O2 production. Major conclusions: The glutathione pool redox state is linked to the availability of H2O2, making glutathionylation an ideal mechanism for preventing oxidative distress whilst playing a part in desensitizing mitochondrial redox signals. General Significance: The biological significance of glutathionylation is rooted in redox status communication. The present review critically evaluates the experimental evidence supporting its role in negating mitochondrial H2O2 production for cell signaling and prevention of electrophilic stress. Full article
(This article belongs to the Special Issue Oxidative Eustress and Distress: Mitochondrial Reactive Oxygen Species in Health and Disease)
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