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Antioxidants
Special Issues
Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—2nd Edition
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Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—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 July 2024 | Viewed by 4257

Special Issue Editors

Dr. Gina Cavaliere

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, University of Perugia, 06126 Perugia, Italy
Interests: metabolic diseases; nutrition; obesity; mitochondrial function; reactive oxygen species; oxidative metabolism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Maria Pina Mollica

E-Mail Website
Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: oxidative metabolism; nutrition; obesity; metaflammation; mitochondrial function; aging; insulin resistance
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanna Trinchese

E-Mail Website
Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: nutrition; metabolic efficiency; obesity; inflammation; mitochondrial function; oxidative stress; diet-induced disorders; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are delighted to be organizing Volume 2 of this Special Issue, entitled “Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases”, especially given the success of Volume 1, which you can read here:

https://www.mdpi.com/journal/antioxidants/special_issues/JEF308HCNO.

Mitochondria are organelles involved in cellular processes including energy production through the oxidative phosphorylation system and in various critical signaling pathways. Mitochondria are not static entities but are dynamic units that undergo fission and fusion cycles to maintain their structural integrity. They are also the principal site of cellular reactive oxygen species (ROS) production, and an imbalance between the production of ROS and cellular antioxidant defenses leads to alterations to cell homeostasis. It is well known that impaired mitochondrial integrity is associated with the pathogenesis of various metabolic diseases, non-communicable pathologies characterized by inflammatory processes closely related to mitochondrial dysfunction. In recent decades, these organelles have been considered as a target of potential therapeutic approaches for the treatment of various diseases. Moreover, molecules naturally produced by plants and a variety of synthetic compounds are capable of modulating mitochondrial function. This Special Issue aims to collect original research and review articles describing the role of mitochondria in metabolic alterations and the potential therapeutic approaches adopted for improving the impaired functionality of mitochondria. Manuscripts that investigate the influence of the natural or chemical compounds that modulate mitochondrial function and the underlying mechanisms will be considered. This data collection can help redefine preventive and therapeutic strategies in an attempt to prevent and counter the onset of metabolic diseases.

Dr. Gina Cavaliere
Prof. Dr. Maria Pina Mollica
Dr. Giovanna Trinchese
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

  • mitochondria function
  • oxidative processes
  • metabolic diseases
  • reactive oxygen species
  • therapeutic approaches
  • mitochondrial integrity
  • energy production
  • mitochondrial bioenergetic
  • metabolism
  • mitochondrial dynamic

Published Papers (4 papers)

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Research

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18 pages, 15087 KiB  
Article
Increased Diabetes Complications in a Mouse Model of Oxidative Stress Due to ‘Mismatched’ Mitochondrial DNA
by Andrzej S. Januszewski, Rachel Blake, Michael Zhang, Ben Ma, Sushma Anand, Carl A. Pinkert, Darren J. Kelly, Alicia J. Jenkins and Ian A. Trounce
Antioxidants 2024, 13(2), 187; https://doi.org/10.3390/antiox13020187 - 01 Feb 2024
Viewed by 876
Abstract
Associations between chronic diabetes complications and mitochondrial dysfunction represent a subject of major importance, given the diabetes pandemic and high personal and socioeconomic costs of diabetes and its complications. Modelling diabetes complications in inbred laboratory animals is challenging due to incomplete recapitulation of [...] Read more.
Associations between chronic diabetes complications and mitochondrial dysfunction represent a subject of major importance, given the diabetes pandemic and high personal and socioeconomic costs of diabetes and its complications. Modelling diabetes complications in inbred laboratory animals is challenging due to incomplete recapitulation of human features, but offer mechanistic insights and preclinical testing. As mitochondrial-based oxidative stress is implicated in human diabetic complications, herein we evaluate diabetes in a unique mouse model that harbors a mitochondrial DNA from a divergent mouse species (the ‘xenomitochondrial mouse’), which has mild mitochondrial dysfunction and increased oxidative stress. We use the streptozotocin-induced diabetes model with insulin supplementation, with 20-weeks diabetes. We compare C57BL/6 mice and the ‘xenomitochondrial’ mouse, with measures of heart and kidney function, histology, and skin oxidative stress markers. Compared to C57BL/6 mice, the xenomitochondrial mouse has increased diabetic heart and kidney damage, with cardiac dysfunction, and increased cardiac and renal fibrosis. Our results show that mitochondrial oxidative stress consequent to divergent mtDNA can worsen diabetes complications. This has implications for novel therapeutics to counter diabetes complications, and for genetic studies of risk, as mtDNA genotypes may contribute to clinical outcomes. Full article
(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—2nd Edition)
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17 pages, 2061 KiB  
Article
High Sucrose Diet-Induced Subunit I Tyrosine 304 Phosphorylation of Cytochrome c Oxidase Leads to Liver Mitochondrial Respiratory Dysfunction in the Cohen Diabetic Rat Model
by Tasnim Arroum, Lucynda Pham, Taryn E. Raisanen, Paul T. Morse, Junmei Wan, Jamie Bell, Rachel Lax, Ann Saada, Maik Hüttemann and Sarah Weksler-Zangen
Antioxidants 2024, 13(1), 19; https://doi.org/10.3390/antiox13010019 - 21 Dec 2023
Viewed by 832
Abstract
The mitochondrial oxidative phosphorylation process generates most of the cellular energy and free radicals in mammalian tissues. Both factors play a critical role in numerous human diseases that could be affected by reversible phosphorylation events that regulate the function and activity of the [...] Read more.
The mitochondrial oxidative phosphorylation process generates most of the cellular energy and free radicals in mammalian tissues. Both factors play a critical role in numerous human diseases that could be affected by reversible phosphorylation events that regulate the function and activity of the oxidative phosphorylation complexes. In this study, we analyzed liver mitochondria of Cohen diabetes-sensitive (CDs) and Cohen diabetes-resistant (CDr) rats, using blue native gel electrophoresis (BN-PAGE) in combination with mitochondrial activity measurements and a site-specific tyrosine phosphorylation implicated in inflammation, a known driver of diabetes pathology. We uncovered the presence of a specific inhibitory phosphorylation on tyrosine 304 of catalytic subunit I of dimeric cytochrome c oxidase (CcO, complex IV). Driven by a high sucrose diet in both CDr and CDs rats, Y304 phosphorylation, which occurs close to the catalytic oxygen binding site, correlates with a decrease in CcO activity and respiratory dysfunction in rat liver tissue under hyperglycemic conditions. We propose that this phosphorylation, specifically seen in dimeric CcO and induced by high sucrose diet-mediated inflammatory signaling, triggers enzymatic activity decline of complex IV dimers and the assembly of supercomplexes in liver tissue as a molecular mechanism underlying a (pre-)diabetic phenotype. Full article
(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—2nd Edition)
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20 pages, 5073 KiB  
Article
Chronic Intermittent Hypoxia-Induced Dysmetabolism Is Associated with Hepatic Oxidative Stress, Mitochondrial Dysfunction and Inflammation
by Joana L. Fernandes, Fátima O. Martins, Elena Olea, Jesus Prieto-Lloret, Patrícia C. Braga, Joana F. Sacramento, Catarina O. Sequeira, Ana P. Negrinho, Sofia A. Pereira, Marco G. Alves, Asunción Rocher and Silvia V. Conde
Antioxidants 2023, 12(11), 1910; https://doi.org/10.3390/antiox12111910 - 25 Oct 2023
Cited by 1 | Viewed by 1153
Abstract
The association between obstructive sleep apnea (OSA) and metabolic disorders is well-established; however, the underlying mechanisms that elucidate this relationship remain incompletely understood. Since the liver is a major organ in the maintenance of metabolic homeostasis, we hypothesize that liver dysfunction plays a [...] Read more.
The association between obstructive sleep apnea (OSA) and metabolic disorders is well-established; however, the underlying mechanisms that elucidate this relationship remain incompletely understood. Since the liver is a major organ in the maintenance of metabolic homeostasis, we hypothesize that liver dysfunction plays a crucial role in the pathogenesis of metabolic dysfunction associated with obstructive sleep apnea (OSA). Herein, we explored the underlying mechanisms of this association within the liver. Experiments were performed in male Wistar rats fed with a control or high fat (HF) diet (60% lipid-rich) for 12 weeks. Half of the groups were exposed to chronic intermittent hypoxia (CIH) (30 hypoxic (5% O2) cycles, 8 h/day) that mimics OSA, in the last 15 days. Insulin sensitivity and glucose tolerance were assessed. Liver samples were collected for evaluation of lipid deposition, insulin signaling, glucose homeostasis, hypoxia, oxidative stress, antioxidant defenses, mitochondrial biogenesis and inflammation. Both the CIH and HF diet induced dysmetabolism, a state not aggravated in animals submitted to HF plus CIH. CIH aggravates hepatic lipid deposition in obese animals. Hypoxia-inducible factors levels were altered by these stimuli. CIH decreased the levels of oxidative phosphorylation complexes in both groups and the levels of SOD-1. The HF diet reduced mitochondrial density and hepatic antioxidant capacity. The CIH and HF diet produced alterations in cysteine-related thiols and pro-inflammatory markers. The results obtained suggest that hepatic mitochondrial dysfunction and oxidative stress, leading to inflammation, may be significant factors contributing to the development of dysmetabolism associated with OSA. Full article
(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—2nd Edition)
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Review

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18 pages, 910 KiB  
Review
Beneficial Effects of Halogenated Anesthetics in Cardiomyocytes: The Role of Mitochondria
by José Luis Guerrero-Orriach, María Dolores Carmona-Luque and Aida Raigón-Ponferrada
Antioxidants 2023, 12(10), 1819; https://doi.org/10.3390/antiox12101819 - 30 Sep 2023
Viewed by 978
Abstract
In the last few years, the use of anesthetic drugs has been related to effects other than those initially related to their fundamental effect, hypnosis. Halogenated anesthetics, mainly sevoflurane, have been used as a therapeutic tool in patients undergoing cardiac surgery, thanks to [...] Read more.
In the last few years, the use of anesthetic drugs has been related to effects other than those initially related to their fundamental effect, hypnosis. Halogenated anesthetics, mainly sevoflurane, have been used as a therapeutic tool in patients undergoing cardiac surgery, thanks to the beneficial effect of the cardiac protection they generate. This effect has been described in several research studies. The mechanism by which they produce this effect has been associated with the effects generated by anesthetic preconditioning and postconditioning. The mechanisms by which these effects are induced are directly related to the modulation of oxidative stress and the cellular damage generated by the ischemia/reperfusion procedure through the overexpression of different enzymes, most of them included in the Reperfusion Injury Salvage Kinase (RISK) and the Survivor Activating Factor Enhancement (SAFE) pathways. Mitochondria is the final target of the different routes of pre- and post-anesthetic conditioning, and it is preserved from the damage generated in moments of lack of oxygen and after the recovery of the normal oxygen concentration. The final consequence of this effect has been related to better cardiac function in this type of patient, with less myocardial damage, less need for inotropic drugs to achieve normal myocardial function, and a shorter hospital stay in intensive care units. The mechanisms through which mitochondrial homeostasis is maintained and its relationship with the clinical effect are the basis of our review. From a translational perspective, we provide information regarding mitochondrial physiology and physiopathology in cardiac failure and the role of halogenated anesthetics in modulating oxidative stress and inducing myocardial conditioning. Full article
(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases—2nd Edition)
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