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: 30 November 2024 | Viewed by 1070

Special Issue Editors


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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
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

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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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Published Papers (1 paper)

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Research

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
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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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