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Redox Homeostasis and Antioxidant Strategies in the Pathophysiology

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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 (15 October 2023) | Viewed by 11886

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Special Issue Editors

Dr. Alessia Remigante

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Guest Editor

Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: human physiology; cell physiology; membrane transport systems; bioactive compound; oxidative stress; human health
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Rossana Morabito

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Guest Editor

Dr. Marika Cordaro

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Guest Editor

Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy
Interests: oxidative stress; nutrition; cell physiology; animal model; inflammation; molecular pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is frequently described as the balance between the production of reactive species, including oxygen and nitrogen, in biological systems and the ability of the latter to defend through sophisticated antioxidant machinery. Nevertheless, when oxidants are produced in excess, or when the antioxidant defenses that regulate them are ineffective, this balance can be perturbed, thus resulting in oxidative conditions, associated with chronic pathogenesis diseases. A certain amount of oxidative stress is useful to the body for growth and cell signaling, but excess levels, produced by several endogenous and exogenous processes, have deleterious effects on cell components including proteins lipids and nucleic acids and alter the redox status of the cell. Antioxidants may protect against cell damage during oxidative stress. New research showed that natural antioxidants in foods have commonly belonged to better health and life quality. Dietary or natural antioxidants play an important role in helping endogenous antioxidants in scavenging excess free radicals. Antioxidant supplements include several important substances (carotenoids, polyphenols, phycocyanin and flavonoids), which are rich in vegetables, fruits and natural foods.
This Special Issue will focus on the investigation of the molecular mechanisms underlying oxidative stress, and pathophysiological consequences in cell and tissue function, in order to open new avenues in therapy. To this aim, the beneficial effects of antioxidants and possible mechanisms of cell adaptation in the context of the imbalance of chronic oxidative-related diseases will be worthy of note. It welcomes manuscripts collecting and contributing to the dissemination of high-quality research articles, as well as review articles, focusing on the relationship between oxidative stress and cellular responses in chronic diseases. In addition, molecular targets of cellular membranes, as well as their potential modulation under oxidative stress will be also considered, in an attempt to provide more information about cell response to oxidative stress and its possible modulation by novel antioxidant strategies. Studies using animal or cell models, as well as clinical studies are welcomed.

Potential topics include but are not limited to the following:

Human health and diseases
Cellular response to oxidative stress
Oxidative stress and related cell signaling
Cell adaptation to oxidative stress
Biomarkers of oxidative stress in diseases
Beneficial effects of natural or synthetic antioxidants in oxidative stress-related diseases
Aging

Dr. Alessia Remigante
Dr. Rossana Morabito
Dr. Marika Cordaro
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.

Published Papers (6 papers)

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Editorial

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4 pages, 168 KiB

Open AccessEditorial

Redox Homeostasis and Antioxidant Strategies in the Pathophysiology

by Alessia Remigante, Marika Cordaro and Rossana Morabito

Antioxidants 2024, 13(3), 281; https://doi.org/10.3390/antiox13030281 - 26 Feb 2024

Viewed by 829

Abstract

The molecular mechanisms underlying oxidative stress, and pathophysiological consequences in cell and tissue function, are frequently described as the imbalance between the production of reactive species and the ability to defend through sophisticated antioxidant machinery (Contributions 1–3) [...] Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

Research

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13 pages, 2878 KiB

Open AccessArticle

Components of the Glutathione Cycle as Markers of Biological Age: An Approach to Clinical Application in Aging

by Estefania Diaz-Del Cerro, Irene Martinez de Toda, Judith Félix, Adriana Baca and Monica De la Fuente

Antioxidants 2023, 12(8), 1529; https://doi.org/10.3390/antiox12081529 - 30 Jul 2023

Cited by 1 | Viewed by 1366

Abstract

The oxidative-inflammatory theory of aging states that aging is the result of the establishment of a chronic oxidative-inflammatory stress situation in which the immune system is implicated. Among the redox parameters, those involved in the glutathione cycle have been suggested as essential in aging. Thus, the first objective of this study was to determine if several components of the glutathione cycle (glutathione reductase (GR) and glutathione peroxidase (GPx) activities, and concentrations of oxidized glutathione (GSSG) and reduced glutathione (GSH)) in leukocytes) are associated with the biological age (ImmunolAge) estimated using the Immunity Clock in 190 men and women. The second objective was to identify the best blood fraction (whole blood, blood cells, erythrocytes, or plasma) to quantify these components and correlate them with the estimated ImmunolAge. The results show that the oxidative state of peripheral leukocytes correlates with their functionality, supporting the idea that this is the basis of immunosenescence. In blood, the correlations are more significant in the fraction of blood cells with respect to ImmunolAge (positive correlations with GSSG concentration and the GSSG/GSH ratio, and negative correlations with GPx and GR activities). Therefore, blood cells are proposed as the most effective sample to estimate the biological age of individuals in clinical settings. Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

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14 pages, 2180 KiB

Open AccessArticle

Global Oxidative Status Is Linked to Calcific Aortic Stenosis: The Differences Due to Diabetes Mellitus and the Effects of Metformin

by Nerea Corbacho-Alonso, Elena Rodríguez-Sánchez, Tamara Sastre-Oliva, Elisa Mercado-García, Ines Perales-Sánchez, Cristina Juarez-Alia, Luis F. López-Almodovar, Luis R. Padial, Teresa Tejerina, Laura Mourino-Alvarez, Gema Ruiz-Hurtado and María G. Barderas

Antioxidants 2023, 12(5), 1024; https://doi.org/10.3390/antiox12051024 - 28 Apr 2023

Cited by 1 | Viewed by 1608

Abstract

Calcific aortic stenosis (CAS) and type 2 diabetes mellitus (T2DM) are related and often concomitant pathologies, accompanied by common comorbidities such as hypertension or dyslipidemia. Oxidative stress is one of the mechanisms that trigger CAS, and it can drive the vascular complications in T2DM. Metformin can inhibit oxidative stress, yet its effects have not been studied in the context of CAS. Here, we assessed the global oxidative status in plasma from patients with CAS, both alone and with T2DM (and under treatment with metformin), using multimarker scores of systemic oxidative damage (OxyScore) and antioxidant defense (AntioxyScore). The OxyScore was determined by measuring carbonyls, oxidized LDL (oxLDL), 8-hydroxy-20-deoxyguanosine (8-OHdG), and xanthine oxidase (XOD) activity. In contrast, the AntioxyScore was determined through the catalase (CAT) and superoxide dismutase (SOD) activity, as well as the total antioxidant capacity (TAC). Patients with CAS displayed enhanced oxidative stress compared to control subjects, probably exceeding their antioxidant capacity. Interestingly, patients with CAS and T2DM displayed less oxidative stress, possibly due to the benefits of their pharmacological therapy (metformin). Thus, reducing oxidative stress or enhancing antioxidant capacity through specific therapies could be a good strategy to manage CAS, focusing on personalized medicine. Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

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14 pages, 3124 KiB

Open AccessArticle

Aldo-Keto Reductase 1C15 Characterization and Protection in Ischemic Brain Injury

by Tuo Yang, Qianqian Li, George Fadoul, Nour Alraqmany, Milos Ikonomovic and Feng Zhang

Antioxidants 2023, 12(4), 909; https://doi.org/10.3390/antiox12040909 - 11 Apr 2023

Cited by 2 | Viewed by 1752

Abstract

Aldo-keto reductase (AKR) 1C15, a member of the AKR superfamily, was recently identified and cloned, and reported to alleviate oxidative stress in endothelial cells in rodent lungs. However, its expression and role in the brain and ischemic brain diseases have not been investigated. AKR1C15 expression was detected with real-time PCR. Mouse ischemic stroke and ischemic preconditioning (IPC) were established with middle cerebral artery occlusion (MCAO) for 1 h or 12 min, respectively. Recombinant AKR1C15 was administered intraperitoneally, and stroke outcome was evaluated with neurobehavioral tests and infarct volumes. Rat primary brain cell cultures were subjected to oxygen–glucose deprivation (OGD) to mimic ischemic injury. Cell survival or in vitro blood–brain barrier (BBB) permeability was measured, and nitric oxide (NO) release was detected. Immunostaining and Western blotting were used to evaluate oxidative-stress-related protein expression. AKR1C15 administration decreased the infarct volume and neurological deficits 2d post-stroke, and its early (1-h) administration after IPC abolished the protection of IPC against stroke. In rat primary brain cell cultures, AKR1C15 was most abundantly expressed in brain microvascular endothelial cells (BMVECs) and microglia. Its expression decreased upon OGD in most cell types except for BMVECs and microglia. In primary neuronal cultures, AKR1C15 treatment prevented OGD-induced cell death accompanied by decreased levels of 4-hydroxynonenal, 8-hydroxy-2′-deoxyguanosine, and heme oxygenase-1. In BMVEC cultures, AKR1C15 treatment protected against OGD-induced cell death and in vitro BBB leakage. In primary microglial cultures, AKR1C15 reduced the release of NO upon proinflammatory stimulation. Our results provide a characterization of the novel antioxidant AKR1C15 and demonstrate its protective role against ischemic injury, both in vivo and in vitro. AKR1C15 may be a promising agent for ischemic stroke treatment. Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

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15 pages, 3226 KiB

Open AccessArticle

Aging Injury Impairs Structural Properties and Cell Signaling in Human Red Blood Cells; Açaì Berry Is a Keystone

by Sara Spinelli, Elisabetta Straface, Lucrezia Gambardella, Daniele Caruso, Giuseppe Falliti, Alessia Remigante, Angela Marino and Rossana Morabito

Antioxidants 2023, 12(4), 848; https://doi.org/10.3390/antiox12040848 - 1 Apr 2023

Cited by 10 | Viewed by 1555

Abstract

Red blood cell (RBC) deformability is the ability of cells to modulate their shape to ensure transit through narrow capillaries of the microcirculation. A loss of deformability can occur in several pathological conditions, during natural RBC aging through an increase in membrane protein phosphorylation, and/or through the structural rearrangements of cytoskeletal proteins due to oxidative conditions, with a key role played by band 3. Due to the close relationship between aging and oxidative stress, flavonoid-rich foods are good candidates to counteract age-related alterations. This study aims to verify the beneficial role of Açaì extract in a d-Galactose (d-Gal)-induced model of aging in human RBCs. To this end, band 3 phosphorylation and structural rearrangements in membrane cytoskeleton-associated proteins, namely spectrin, ankyrin, and/or protein 4.1, are analyzed in RBCs treated with 100 mM d-Gal for 24 h, with or without pre-incubation with 10 μg/mL Açaì extract for 1 h. Furthermore, RBC deformability is also measured. Tyrosine phosphorylation of band 3, membrane cytoskeleton-associated proteins, and RBC deformability (elongation index) are analyzed using western blotting analysis, FACScan flow cytometry, and ektacytometry, respectively. The present data show that: (i) Açaì berry extract restores the increase in band 3 tyrosine phosphorylation and Syk kinase levels after exposure to 100 mM d-Gal treatment; and (ii) Açaì berry extract partially restores alterations in the distribution of spectrin, ankyrin, and protein 4.1. Interestingly, the significant decrease in membrane RBC deformability associated with d-Gal treatment is alleviated by pre-treatment with Açaì extract. These findings further contribute to clarify mechanisms of natural aging in human RBCs, and propose flavonoid substances as potential natural antioxidants for the treatment and/or prevention of oxidative-stress-related disease risk. Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

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Review

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19 pages, 1065 KiB

Open AccessReview

Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease

by Karina-Alexandra Cojocaru, Ionut Luchian, Ancuta Goriuc, Lucian-Mihai Antoci, Cristian-Gabriel Ciobanu, Roxana Popescu, Cristiana-Elena Vlad, Mihaela Blaj and Liliana Georgeta Foia

Antioxidants 2023, 12(3), 658; https://doi.org/10.3390/antiox12030658 - 7 Mar 2023

Cited by 18 | Viewed by 4198

Abstract

Mitochondria are subcellular organelles involved in essential cellular functions, including cytosolic calcium regulation, cell apoptosis, and reactive oxygen species production. They are the site of important biochemical pathways, including the tricarboxylic acid cycle, parts of the ureagenesis cycle, or haem synthesis. Mitochondria are responsible for the majority of cellular ATP production through OXPHOS. Mitochondrial dysfunction has been associated with metabolic pathologies such as diabetes, obesity, hypertension, neurodegenerative diseases, cellular aging, and cancer. In this article, we describe the pathophysiological changes in, and mitochondrial role of, metabolic disorders (diabetes, obesity, and cardiovascular disease) and their correlation with oxidative stress. We highlight the genetic changes identified at the mtDNA level. Additionally, we selected several representative biomarkers involved in oxidative stress and summarize the progress of therapeutic strategies. Full article

(This article belongs to the Special Issue Redox Homeostasis and Antioxidant Strategies in the Pathophysiology)

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