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Oxygen
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Mitochondrial Oxidative Stress in Health and Disease
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Mitochondrial Oxidative Stress in Health and Disease

A special issue of Oxygen (ISSN 2673-9801).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 6585

Special Issue Editors

Dr. Anna Atlante

E-Mail Website
Guest Editor
Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies (IBIOM)-CNR, Via G. Amendola122/O, 70126 Bari, Italy
Interests: mitochondrial bioenergetics; oxidative phosphorylation; mitochondrial dysfunction; metabolic regulation; oxidative stress; apoptosis; Alzheimer’s disease; cystic fibrosis
Special Issues, Collections and Topics in MDPI journals
Dr. Daniela Valenti

E-Mail Website
Guest Editor
Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, Bari, Italy
Interests: mitochondrial bioenergetics; mitochondrial metabolism; mitochondrial transport; mitochondrial signaling pathways; mitochondrial dysfunction; neurodevelopmental diseases; oxidative stress; reactive oxygen species; programmed cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria produce reactive oxygen species (ROS) as a natural by-product of electron transport chain activity.

In physiological conditions, the production of ROS, involved in regulating the activity of many key enzymes, is efficiently neutralized by antioxidant pathways, which regulates oxygen consumption and redox generation capacity.

In pathological conditions, excessive generation of ROS can elicit an intracellular state known as oxidative stress, when cellular antioxidant systems are no longer able to maintain physiological redox homeostasis.

This Special Issue of Oxygen, entitled “Mitochondrial Oxidative Stress in Health and Disease”, aims to cover the more recent advances and insights into research in these areas, ranging from biochemistry to pathophysiology, and will focus on little-studied aspects of mitochondrial oxidative stress which may help develop new health and medical applications.

I look forward to receiving your contributions.

Dr. Anna Atlante
Dr. Daniela Valenti
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. Oxygen is an international peer-reviewed open access quarterly 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 1000 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

  • oxidative stress
  • mitochondria
  • reactive oxygen species production
  • bioenergetics
  • mitochondrial dysfunction
  • respiratory chain
  • oxidative phosphorylation
  • mitochondrial permeability transition
  • redox signaling
  • antioxidants
  • neurodegenerative diseases
  • autophagy
  • cell death

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Published Papers (3 papers)

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Research

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9 pages, 1586 KiB  
Article
Expansion of Electron Transport Chain Mutants That Cause Anesthetic-Induced Toxicity in Drosophila melanogaster
by Luke A. Borchardt, Zachariah P. G. Olufs, Philip G. Morgan, David A. Wassarman and Misha Perouansky
Oxygen 2024, 4(1), 108-116; https://doi.org/10.3390/oxygen4010006 - 2 Mar 2024
Viewed by 884
Abstract
The mitochondrial electron transport chain (mETC) contains molecular targets of volatile general anesthetics (VGAs), which places individuals with mETC mutations at risk for anesthetic complications, as exemplified by patients with Leigh syndrome (LS). The Drosophila melanogaster homozygous mutant for ND-23, which encodes [...] Read more.
The mitochondrial electron transport chain (mETC) contains molecular targets of volatile general anesthetics (VGAs), which places individuals with mETC mutations at risk for anesthetic complications, as exemplified by patients with Leigh syndrome (LS). The Drosophila melanogaster homozygous mutant for ND-23, which encodes a subunit of mETC Complex I, replicates numerous characteristics of LS, including neurodegeneration, shortened lifespan, behavioral anesthetic hypersensitivity, and toxicity. The anesthetic phenotype of toxicity (lethality) is also observed in flies homozygous for mutations in other Complex I subunits. By contrast, mutations conferring sensitivity have not yet been identified for subunits of Complexes II–V. Furthermore, anesthetic phenotypes are thought to be recessive; that is, risk is not conferred by heterozygous mutations. However, at older ages, exposure of heterozygous mutant ND-23 flies to the VGA isoflurane in 75% oxygen (hyperoxia) results in toxicity. It is also unknown whether combinations of heterozygous mutations in different subunits of the mETC can result in anesthetic toxicity. Here, we show that, following exposure to isoflurane in hyperoxia, flies carrying heterozygous mutations in two Complex I subunits, ND-23 and ND-SGDH (NADH dehydrogenase (ubiquinone) SGDH subunit), had a level of anesthetic toxicity that exceeded the added toxicities of the individual heterozygous mutations. In addition, we show that flies heterozygous for two different alleles of the Complex II gene SdhB were susceptible to isoflurane/hyperoxia-induced anesthetic toxicity. Finally, a mutation in the SdhC subunit of Complex II of Caenorhabditis elegans resulted in isoflurane-induced mortality, supporting the role of Complex II in anesthetic toxicity. These data expand the landscape of mutations in the mETC that increase sensitivity to anesthetic toxicity. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Health and Disease)
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Review

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13 pages, 969 KiB  
Review
Mitochondrial Dysfunction and Nanocarrier-Based Treatments in Chronic Obstructive Pulmonary Disease (COPD)
by Kiyoshi Sato and Hiroyoshi Kawakami
Oxygen 2023, 3(4), 394-406; https://doi.org/10.3390/oxygen3040026 - 14 Nov 2023
Cited by 2 | Viewed by 1528
Abstract
Mitochondrial dysfunction significantly contributes to the pathogenesis and progression of chronic obstructive pulmonary disease (COPD). To treat mitochondrial dysfunction in COPD, novel drug delivery systems (DDS) are needed. In this review, we provide a brief overview of the current understanding of the factors [...] Read more.
Mitochondrial dysfunction significantly contributes to the pathogenesis and progression of chronic obstructive pulmonary disease (COPD). To treat mitochondrial dysfunction in COPD, novel drug delivery systems (DDS) are needed. In this review, we provide a brief overview of the current understanding of the factors in COPD and highlight the trends in novel nanocarriers/nanoparticles for targeting mitochondrial dysfunction. These drug-encapsulated nanoparticles are still in the early stages of clinical application but represent the most promising system for COPD therapy. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Health and Disease)
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16 pages, 1225 KiB  
Review
Mechanisms of Mitochondrial Oxidative Stress in Brain Injury: From Pathophysiology to Therapeutics
by Andrew Nguyen, Anjali B. Patel, Ivelina P. Kioutchoukova, Michael J. Diaz and Brandon Lucke-Wold
Oxygen 2023, 3(2), 163-178; https://doi.org/10.3390/oxygen3020012 - 7 Apr 2023
Cited by 4 | Viewed by 3387
Abstract
Mitochondrial oxidative stress has been implicated in various forms of brain injury, both traumatic and non-traumatic. Due to its oxidative demand, the brain is intimately dependent on its mitochondrial functioning. However, there remains appreciable heterogeneity in the development of these injuries regarding ROS [...] Read more.
Mitochondrial oxidative stress has been implicated in various forms of brain injury, both traumatic and non-traumatic. Due to its oxidative demand, the brain is intimately dependent on its mitochondrial functioning. However, there remains appreciable heterogeneity in the development of these injuries regarding ROS and their effect on the sequelae. These include traumatic insults such as TBIs and intracranial hemorrhaging secondary to this. In a different vein, such injuries may be attributed to other etiologies such as infection, neoplasm, or spontaneous hemorrhage (strokes, aneurysms). Clinically, the manner of treatment may also be adjusted in relation to each injury and its unique progression in the context of ROS. In the current review, then, the authors highlight the role of mitochondrial ROS in various forms of brain injury, emphasizing both the collective and unique elements of each form. Lastly, these narratives are met with the current therapeutic landscape and the role of emerging therapies in treating reactive oxygen species in brain injuries. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Health and Disease)
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