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Antioxidants
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Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition
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Mitochondrial Oxidative Stress in Aging and Disease—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: closed (30 March 2025) | Viewed by 8959

Special Issue Editors

Dr. Angela Maria Serena Lezza

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Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: aging; mitochondrial biogenesis in aging; mitochondrial pathologies; pathologies with mitochondrial oxidative stress (age-related diseases, autoimmune and inflammatory pathologies, neurodegenerative diseases); calorie restriction and nutritional anti-aging interventions; mtDNA–TFAM relationships
Special Issues, Collections and Topics in MDPI journals
Dr. Vito Pesce

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: mtDNA damage and deletions; mitochondrial oxidative stress and antioxidant defense; mitochondrial biogenesis and dynamics; mitochondrial quality control; mitochondrial dysfunction in aging and age-related degenerative disorders; nutritional anti-aging interventions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are the main hub of cellular oxidative stress, as most Reactive Oxygen Species (ROS) are generated as byproducts of the mitochondrial electron transport chain. With research progress, the role of ROS has shifted from the initial consideration only as damaging agents to the recent one as intracellular messengers, necessary for physiological functions but toxic at high levels. Therefore, when the usual ROS-neutralizing action, performed by the antioxidant defense systems, is no longer adequately efficient to counteract the age-related increased production of mitochondrial ROS, oxidative stress originates inside the organelles, leading to a dual effect: the disruption of redox signaling and the production of oxidative damage. Redox signaling dysregulation occurs through changes in enzymes and transcription factors that are sensitive to the redox state. Oxidative damage arises when ROS react with nearby biomolecules, resulting in oxidatively modified products and generating harmful effects in mitochondria and the cellular environment. The levels of ROS increase gradually throughout the lifespan, impairing mitochondrial function and affecting all tissues dependent on the organelle’s production of energy and substrates, thus heavily contributing to the aging process. The natural phenomenon of aging features gradual changes in cell and mitochondrial functionality, originating from a blend of genetic, environmental and lifestyle factors, among which oxidative stress emerges as a major driver. Mitochondrial oxidative stress, directly or eliciting inflammation, ultimately results in age-related inflammatory and degenerative diseases, which have become the most common health threat nowadays. Various kinds of interventions, aiming to delay or to prevent the development of mitochondrial oxidative stress, have been proposed or are under actual study and represent a valuable and multifaceted therapeutical approach for such diseases. Therefore, the goal of this Special Issue is to deliver a broad and updated overview of experimental models, molecular mechanisms and therapeutic options useful to tackle the involvement of “mitochondrial oxidative stress in aging and disease” through contributions by experts of the field in the form of research papers and critical reviews.

Dr. Angela Maria Serena Lezza
Dr. Vito Pesce
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

  • mitochondrial oxidative stress in aging
  • mitochondrial oxidative stress in age-related or metabolic diseases
  • mitochondrial signaling via ROS in diseases
  • mitochondrial oxidative stress and genomic instability
  • mitochondrial oxidative stress and inflammation
  • antioxidants as novel therapeutic approaches
  • mitochondrial pathologies
  • aging
  • mitochondrial

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Related Special Issue

Published Papers (6 papers)

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Research

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25 pages, 10658 KiB  
Article
Dysfunctional Mitochondria Characterize Amyotrophic Lateral Sclerosis Patients’ Cells Carrying the p.G376D TARDBP Pathogenetic Substitution
by Giuseppe Petito, Victoria Stefania Del Fiore, Arianna Cuomo, Federica Cioffi, Gilda Cobellis, Antonia Lanni, Flora Guerra, Cecilia Bucci, Rosalba Senese and Roberta Romano
Antioxidants 2025, 14(4), 401; https://doi.org/10.3390/antiox14040401 - 28 Mar 2025
Viewed by 475
Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease caused by the degeneration of upper and lower motor neurons in the brain, brainstem and spinal cord. About 10% of familial ALS cases are linked to pathogenetic substitution in TARDBP, the gene encoding the [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease caused by the degeneration of upper and lower motor neurons in the brain, brainstem and spinal cord. About 10% of familial ALS cases are linked to pathogenetic substitution in TARDBP, the gene encoding the TDP-43 protein. A novel rare causative variant in TARDBP (p.G376D) was recently reported in ALS patients. It leads to TDP-43 cytoplasmic mislocalization, increased oxidative stress and reduced cell viability. However, functional studies on the effects of this molecular defect have not yet been carried out. Mitochondria are highly dynamic organelles, and their deregulation has emerged as a key factor in many diseases, among which is ALS. Therefore, this study aimed at determining the impact of this causative variant on mitochondria. In cellular models expressing TDP-43G376D and in fibroblasts derived from patients carrying this molecular defect, we observed alterations of mitochondrial functionality. We demonstrated increased localization of the mutated protein to mitochondria and a reduced abundance of subunits of complex I and complex II of the mitochondrial respiratory chain, associated with a decrease in mitochondrial membrane potential, in cellular respiration and in cytochrome C oxidase (COX) activity. Moreover, ALS cells showed increased mitochondrial fragmentation and reduced abundance of antioxidant enzymes causing increased oxidative stress. These results expand our knowledge about the molecular mechanisms underlying ALS pathogenesis associated with TDP-43 p.G376D and could help to identify new therapeutic strategies to counteract this disease. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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17 pages, 2227 KiB  
Article
Synergistic ROS Reduction Through the Co-Inhibition of BRAF and p38 MAPK Ameliorates Senescence
by Myeong Uk Kuk, Duyeol Kim, Yun Haeng Lee, Jee Hee Yoon, Ji Ho Park, Yoo Jin Lee, Byeong Hyeon So, Minseon Kim, Hyung Wook Kwon, Youngjoo Byun and Joon Tae Park
Antioxidants 2024, 13(12), 1465; https://doi.org/10.3390/antiox13121465 - 28 Nov 2024
Cited by 2 | Viewed by 885
Abstract
Reactive oxygen species (ROS)-mediated damage to macromolecules and cellular organelles is one of the major causes of senescence. Therapeutic strategies that lower ROS levels have been proposed as important treatments for senescence, but effective mechanisms for reducing ROS levels have not been discovered. [...] Read more.
Reactive oxygen species (ROS)-mediated damage to macromolecules and cellular organelles is one of the major causes of senescence. Therapeutic strategies that lower ROS levels have been proposed as important treatments for senescence, but effective mechanisms for reducing ROS levels have not been discovered. Here, we aimed to find a combination that has a synergistic effect on ROS reduction using senomorphics known to reduce ROS. Combination treatment with BRAF inhibitor SB590885 and p38 MAPK inhibitor SB203580 showed a synergistic effect on ROS reduction compared to treatment with either drug alone. The synergistic effect of ROS reduction through this combination led to a synergistic effect that restored mitochondrial function and ameliorated senescence-associated phenotypes. To elucidate the underlying mechanism by which the synergistic effect of the two drugs reverses senescence, we performed RNA sequencing and identified metallothionein 2A (MT2A) as a key gene. MT2A was upregulated in response to combination therapy, and overexpression of MT2A led to a decrease in ROS and subsequent recovery of senescence-associated phenotypes, similar to the effects of combination therapy. Taken together, we found a drug combination that showed synergistic effects on ROS reduction, which contributed to the recovery of senescence-associated phenotypes through MT2A gene regulation. This study opens up a new avenue in aging research by demonstrating that combination therapy with existing senomorphics can enhance the ability to reverse senescence and that similar reversal effects can be achieved through gene regulation regulated by combination therapy. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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16 pages, 2291 KiB  
Article
Prevention of Sunlight-Induced Cell Damage by Selective Blue-Violet-Light-Filtering Lenses in A2E-Loaded Retinal Pigment Epithelial Cells
by Coralie Barrau, Mélanie Marie, Camille Ehrismann, Pauline Gondouin, José-Alain Sahel, Thierry Villette and Serge Picaud
Antioxidants 2024, 13(10), 1195; https://doi.org/10.3390/antiox13101195 - 1 Oct 2024
Viewed by 1535
Abstract
Blue light accelerates retinal aging. Previous studies have indicated that wavelengths between 400 and 455 nm are most harmful to aging retinal pigment epithelia (RPE). This study explored whether filtering these wavelengths can protect cells exposed to broad sunlight. Primary porcine RPE cells [...] Read more.
Blue light accelerates retinal aging. Previous studies have indicated that wavelengths between 400 and 455 nm are most harmful to aging retinal pigment epithelia (RPE). This study explored whether filtering these wavelengths can protect cells exposed to broad sunlight. Primary porcine RPE cells loaded with 20 µM A2E were exposed to emulated sunlight filtered through eye media at 1.8 mW/cm2 for 18 h. Filters selectively filtering out light over 400–455 nm and a dark-yellow filter were interposed. Cell damage was measured by apoptosis, hydrogen peroxide (H2O2) production, and mitochondrial membrane potential (MMP). Sunlight exposure increased apoptosis by 2.7-fold and H2O2 by 4.8-fold, and halved MMP compared to darkness. Eye Protect SystemTM (EPS) technology, filtering out 25% of wavelengths over 400–455 nm, reduced apoptosis by 44% and H2O2 by 29%. The Multilayer Optical Film (MOF), at 80% of light filtered, reduced apoptosis by 91% and H2O2 by 69%, and increased MMP by 73%, overpassing the dark-yellow filter. Photoprotection increased almost linearly with blue-violet light filtering (400–455 nm) but not with total blue filtering (400–500 nm). Selective filters filtering out 25% (EPS) to 80% (MOF) of blue-violet light offer substantial protection without affecting perception or non-visual functions, making them promising for preventing light-induced retinal damage with aesthetic acceptance for permanent wear. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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Review

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21 pages, 1694 KiB  
Review
Molecular Insights in the Anticancer Activity of Natural Tocotrienols: Targeting Mitochondrial Metabolism and Cellular Redox Homeostasis
by Raffaella Chiaramonte, Giulia Sauro, Domenica Giannandrea, Patrizia Limonta and Lavinia Casati
Antioxidants 2025, 14(1), 115; https://doi.org/10.3390/antiox14010115 - 20 Jan 2025
Viewed by 1181
Abstract
The role of mitochondria as the electric engine of cells is well established. Over the past two decades, accumulating evidence has pointed out that, despite the presence of a highly active glycolytic pathway (Warburg effect), a functional and even upregulated mitochondrial respiration occurs [...] Read more.
The role of mitochondria as the electric engine of cells is well established. Over the past two decades, accumulating evidence has pointed out that, despite the presence of a highly active glycolytic pathway (Warburg effect), a functional and even upregulated mitochondrial respiration occurs in cancer cells to meet the need of high energy and the biosynthetic demand to sustain their anabolic growth. Mitochondria are also the primary source of intracellular ROS. Cancer cells maintain moderate levels of ROS to promote tumorigenesis, metastasis, and drug resistance; indeed, once the cytotoxicity threshold is exceeded, ROS trigger oxidative damage, ultimately leading to cell death. Based on this, mitochondrial metabolic functions and ROS generation are considered attractive targets of synthetic and natural anticancer compounds. Tocotrienols (TTs), specifically the δ- and γ-TT isoforms, are vitamin E-derived biomolecules widely shown to possess striking anticancer properties since they regulate several intracellular molecular pathways. Herein, we provide for the first time an overview of the mitochondrial metabolic reprogramming and redox homeostasis perturbation occurring in cancer cells, highlighting their involvement in the anticancer properties of TTs. This evidence sheds light on the use of these natural compounds as a promising preventive or therapeutic approach for novel anticancer strategies. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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32 pages, 2811 KiB  
Review
The Neural Palette of Heme: Altered Heme Homeostasis Underlies Defective Neurotransmission, Increased Oxidative Stress, and Disease Pathogenesis
by Adedamola Saidi Soladogun and Li Zhang
Antioxidants 2024, 13(12), 1441; https://doi.org/10.3390/antiox13121441 - 22 Nov 2024
Cited by 1 | Viewed by 1731
Abstract
Heme, a complex iron-containing molecule, is traditionally recognized for its pivotal role in oxygen transport and cellular respiration. However, emerging research has illuminated its multifaceted functions in the nervous system, extending beyond its canonical roles. This review delves into the diverse roles of [...] Read more.
Heme, a complex iron-containing molecule, is traditionally recognized for its pivotal role in oxygen transport and cellular respiration. However, emerging research has illuminated its multifaceted functions in the nervous system, extending beyond its canonical roles. This review delves into the diverse roles of heme in the nervous system, highlighting its involvement in neural development, neurotransmission, and neuroprotection. We discuss the molecular mechanisms by which heme modulates neuronal activity and synaptic plasticity, emphasizing its influence on ion channels and neurotransmitter receptors. Additionally, the review explores the potential neuroprotective properties of heme, examining its role in mitigating oxidative stress, including mitochondrial oxidative stress, and its implications in neurodegenerative diseases. Furthermore, we address the pathological consequences of heme dysregulation, linking it to conditions such as Alzheimer’s disease, Parkinson’s disease, and traumatic brain injuries. By providing a comprehensive overview of heme’s multifunctional roles in the nervous system, this review underscores its significance as a potential therapeutic target and diagnostic biomarker for various neurological disorders. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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30 pages, 2650 KiB  
Review
Neuroinflammation in Age-Related Neurodegenerative Diseases: Role of Mitochondrial Oxidative Stress
by Xenia Abadin, Cristina de Dios, Marlene Zubillaga, Elia Ivars, Margalida Puigròs, Montserrat Marí, Albert Morales, Marisa Vizuete, Javier Vitorica, Ramon Trullas, Anna Colell and Vicente Roca-Agujetas
Antioxidants 2024, 13(12), 1440; https://doi.org/10.3390/antiox13121440 - 22 Nov 2024
Cited by 2 | Viewed by 2174
Abstract
A shared hallmark of age-related neurodegenerative diseases is the chronic activation of innate immune cells, which actively contributes to the neurodegenerative process. In Alzheimer’s disease, this inflammatory milieu exacerbates both amyloid and tau pathology. A similar abnormal inflammatory response has been reported in [...] Read more.
A shared hallmark of age-related neurodegenerative diseases is the chronic activation of innate immune cells, which actively contributes to the neurodegenerative process. In Alzheimer’s disease, this inflammatory milieu exacerbates both amyloid and tau pathology. A similar abnormal inflammatory response has been reported in Parkinson’s disease, with elevated levels of cytokines and other inflammatory intermediates derived from activated glial cells, which promote the progressive loss of nigral dopaminergic neurons. Understanding the causes that support this aberrant inflammatory response has become a topic of growing interest and research in neurodegeneration, with high translational potential. It has been postulated that the phenotypic shift of immune cells towards a proinflammatory state combined with the presence of immunogenic cell death fuels a vicious cycle in which mitochondrial dysfunction plays a central role. Mitochondria and mitochondria-generated reactive oxygen species are downstream effectors of different inflammatory signaling pathways, including inflammasomes. Dysfunctional mitochondria are also recognized as important producers of damage-associated molecular patterns, which can amplify the immune response. Here, we review the major findings highlighting the role of mitochondria as a checkpoint of neuroinflammation and immunogenic cell deaths in neurodegenerative diseases. The knowledge of these processes may help to find new druggable targets to modulate the inflammatory response. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative Stress in Aging and Disease—2nd Edition)
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