Special Issue "ROS and COVID"

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: 15 February 2021.

Special Issue Editors

Prof. Dr. Dimitrios Kouretas
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Guest Editor
Department of Biochemistry & Biotechnology , University of Thessaly, 41500 Larissa, Greece
Interests: molecular mechanisms of antioxidant activity of plant phenolics; adaptation in exercise in human: study of redox and molecular mechanisms involved; functional food development and action in humans
Special Issues and Collections in MDPI journals
Dr. Konstantinos Poulas
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Guest Editor
School of Pharmacy, University of Patras, Greece
Interests: laboratory and clinical research on e-cigarettes; toxicological and preclinical studies on non-combustible products; cloning, expression, purification, and biochemical characterization of recombinant fragments; electroceuticals
Special Issues and Collections in MDPI journals
Dr. Konstantinos Farsalinos
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Guest Editor
Department of Pharmacy, University of Patras, GR26500, Patras, Greece
Interests: laboratory and clinical research on e-cigarettes; cytotoxic effects of e-cigarette vapor on cultured cells; effects of e-cigarette use on cardiac function and coronary circulation
Special Issues and Collections in MDPI journals
Prof. Dr. Joanna Floros
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Guest Editor
Center for Host Defense, Inflammation, and Lung Disease (CHILD) Research Department of Pediatrics, The Pennsylvania State University College of Medicine, Hershey, PA, USA

Special Issue Information

Coronavirus disease 2019 (COVID-19) is caused by the novel coronavirus SARS-CoV-2. While the disease is mild in many cases, severe COVID-19 involves a hyper-inflammatory response, commonly called a cytokine storm, characterized by the release of pro-inflammatory cytokines that can lead to acute respiratory distress syndrome and death. It is known that pulmonary immunity in elderly persons is compromised, with impaired innate and adaptive cellular immune responses and reduced function of the lung itself. While overall innate immune responses may decline with age, inflammatory cytokines such as IL-6 and TNF-a, and acute phase reactants such as C-reactive protein, are elevated in older adults, maintaining a low level of chronic inflammation associated with increased levels of oxidative stress which drive the sustained levels of inflammation. Risk factors for severe COVID-19 such as obesity and diabetes are also associated with oxidative stress. Viral entry into the cytoplasm of the lung host epithelial cells results in interactions that affect cell metabolism and induce oxidative stress responses. The resulting inflammation and oxidative stress may have a negative impact on the expression and function of pulmonary surfactant, further compromising gas exchange and surfactant-protein-mediated innate host defense. For this reason, the study of reactive oxidant species (ROS) of all facets (nutrition modalities, supplements administration, redox biomarker study, antioxidant involvement, drug–protein interaction, the genetics of lung innate immune molecules such as the surfactant proteins, and the physiology and/or biochemistry of ROS in COVID-19) is of particular interest and constitutes the scope of the present Special Issue.

Prof. Dr. Dimitrios Kouretas
Dr. Konstantinos Poulas
Dr. Konstantinos Farsalinos
Prof. Dr. Joanna Floros
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 papers will be 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 1600 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 (5 papers)

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Research

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Open AccessArticle
Sex and SP-A2 Dependent NAD(H) Redox Alterations in Mouse Alveolar Macrophages in Response to Ozone Exposure: Potential Implications for COVID-19
Antioxidants 2020, 9(10), 915; https://doi.org/10.3390/antiox9100915 (registering DOI) - 25 Sep 2020
Abstract
Co-enzyme nicotinamide adenine dinucleotide (NAD(H)) redox plays a key role in macrophage function. Surfactant protein (SP-) A modulates the functions of alveolar macrophages (AM) and ozone (O3) exposure in the presence or absence of SP-A and reduces mouse survival in a [...] Read more.
Co-enzyme nicotinamide adenine dinucleotide (NAD(H)) redox plays a key role in macrophage function. Surfactant protein (SP-) A modulates the functions of alveolar macrophages (AM) and ozone (O3) exposure in the presence or absence of SP-A and reduces mouse survival in a sex-dependent manner. It is unclear whether and how NAD(H) redox status plays a role in the innate immune response in a sex-dependent manner. We investigated the NAD(H) redox status of AM from SP-A2 and SP-A knockout (KO) mice in response to O3 or filtered air (control) exposure using optical redox imaging technique. We found: (i) In SP-A2 mice, the redox alteration of AM in response to O3 showed sex-dependence with AM from males being significantly more oxidized and having a higher level of mitochondrial reactive oxygen species than females; (ii) AM from KO mice were more oxidized after O3 exposure and showed no sex differences; (iii) AM from female KO mice were more oxidized than female SP-A2 mice; and (iv) Two distinct subpopulations characterized by size and redox status were observed in a mouse AM sample. In conclusions, the NAD(H) redox balance in AM responds to O3 in a sex-dependent manner and the innate immune molecule, SP-A2, contributes to this observed sex-specific redox response. Full article
(This article belongs to the Special Issue ROS and COVID)
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Open AccessArticle
Adelmidrol: A New Promising Antioxidant and Anti-Inflammatory Therapeutic Tool in Pulmonary Fibrosis
Antioxidants 2020, 9(7), 601; https://doi.org/10.3390/antiox9070601 - 09 Jul 2020
Cited by 1
Abstract
Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known anti-inflammatory and [...] Read more.
Background: Chronic pulmonary diseases are characterized by airway remodeling due to complex multicellular responses and the production of free oxygen radicals. They lead to a progressive decline of pulmonary functions. Adelmidrol is an analogue of palmitoylethanolamide (PEA), which is a well-known anti-inflammatory and anti-oxidant compound. In this study, we investigated the efficacy of adelmidrol (10 mg/Kg) for bleomycin-induced pulmonary fibrosis in mice. Methods: Bleomycin intratracheal administration was performed on the first day and for the following twenty-one days, mice were treated with adelmidrol (10 mg/Kg). Results: The survival rate and body weight gain were recorded daily. At the end of the experiment, adelmidrol-administered animals showed reduced airway infiltration by inflammatory cells, Myeloperoxidase (MPO) activity, and pro-inflammatory cytokine overexpression (IL,6 IL-1β, TNF-α, and TGF-1β). Moreover, adelmidrol treatment was able to manage the significant incapacity of antioxidants and elevation of the oxidant burden, as shown by the MDA, SOD, and GSH levels and decreased nitric oxide production. It was also able to significantly modulate the JAK2/STAT3 and IκBα/NF-kB pathway. Histologic examination of the lung tissues showed reduced sample injury, mast cell degranulation, chymase activity, and collagen deposition. Conclusions: In sum, our results propose adelmidrol as a therapeutic approach in the treatment of pulmonary fibrosis. Full article
(This article belongs to the Special Issue ROS and COVID)
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Review

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Open AccessReview
Oxidative Stress, Proton Fluxes, and Chloroquine/Hydroxychloroquine Treatment for COVID-19
Antioxidants 2020, 9(9), 894; https://doi.org/10.3390/antiox9090894 - 21 Sep 2020
Abstract
Chloroquine (CQ) and hydroxychloroquine (HCQ) have been proposed as treatments for COVID-19. These drugs have been studied for many decades, primarily in the context of their use as antimalarials, where they induce oxidative stress-killing of the malarial parasite. Less appreciated, however, is evidence [...] Read more.
Chloroquine (CQ) and hydroxychloroquine (HCQ) have been proposed as treatments for COVID-19. These drugs have been studied for many decades, primarily in the context of their use as antimalarials, where they induce oxidative stress-killing of the malarial parasite. Less appreciated, however, is evidence showing that CQ/HCQ causes systemic oxidative stress. In vitro and observational data suggest that CQ/HCQ can be repurposed as potential antiviral medications. This review focuses on the potential health concerns of CQ/HCQ induced by oxidative stress, particularly in the hyperinflammatory stage of COVID-19 disease. The pathophysiological role of oxidative stress in acute respiratory distress syndrome (ARDS) has been well-documented. Additional oxidative stress caused by CQ/HCQ during ARDS could be problematic. In vitro data showing that CQ forms a complex with free-heme that promotes lipid peroxidation of phospholipid bilayers are also relevant to COVID-19. Free-heme induced oxidative stress is implicated as a systemic activator of coagulation, which is increasingly recognized as a contributor to COVID-19 morbidity. This review will also provide a brief overview of CQ/HCQ pharmacology with an emphasis on how these drugs alter proton fluxes in subcellular organelles. CQ/HCQ-induced alterations in proton fluxes influence the type and chemical reactivity of reactive oxygen species (ROS). Full article
(This article belongs to the Special Issue ROS and COVID)
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Open AccessReview
The Importance of Redox Status in the Frame of Lifestyle Approaches and the Genetics of the Lung Innate Immune Molecules, SP-A1 and SP-A2, on Differential Outcomes of COVID-19 Infection
Antioxidants 2020, 9(9), 784; https://doi.org/10.3390/antiox9090784 - 25 Aug 2020
Abstract
The pandemic of COVID-19 is of great concern to the scientific community. This mainly affects the elderly and people with underlying diseases. People with obesity are more likely to experience unpleasant disease symptoms and increased mortality. The severe oxidative environment that occurs in [...] Read more.
The pandemic of COVID-19 is of great concern to the scientific community. This mainly affects the elderly and people with underlying diseases. People with obesity are more likely to experience unpleasant disease symptoms and increased mortality. The severe oxidative environment that occurs in obesity due to chronic inflammation permits viral activation of further inflammation leading to severe lung disease. Lifestyle affects the levels of inflammation and oxidative stress. It has been shown that a careful diet rich in antioxidants, regular exercise, and fasting regimens, each and/or together, can reduce the levels of inflammation and oxidative stress and strengthen the immune system as they lead to weight loss and activate cellular antioxidant mechanisms and reduce oxidative damage. Thus, a lifestyle change based on the three pillars: antioxidants, exercise, and fasting could act as a proactive preventative measure against the adverse effects of COVID-19 by maintaining redox balance and well-functioning immunity. Moreover, because of the observed diversity in the expression of COVID-19 inflammation, the role of genetics of innate immune molecules, surfactant protein A (SP-A)1 and SP-A2, and their differential impact on the local lung microenvironment and host defense is reviewed as genetics may play a major role in the diverse expression of the disease. Full article
(This article belongs to the Special Issue ROS and COVID)
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Open AccessReview
The Role of Glutathione in Protecting against the Severe Inflammatory Response Triggered by COVID-19
Antioxidants 2020, 9(7), 624; https://doi.org/10.3390/antiox9070624 - 16 Jul 2020
Cited by 1
Abstract
The novel COVID-19 pandemic is affecting the world’s population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome, whereas in many cases the disease [...] Read more.
The novel COVID-19 pandemic is affecting the world’s population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome, whereas in many cases the disease has a mild or even asymptomatic progression. A common denominator in all conditions associated with COVID-19 appears to be the impaired redox homeostasis responsible for reactive oxygen species (ROS) accumulation; therefore, levels of glutathione (GSH), the key anti-oxidant guardian in all tissues, could be critical in extinguishing the exacerbated inflammation that triggers organ failure in COVID-19. The present review provides a biochemical investigation of the mechanisms leading to deadly inflammation in severe COVID-19, counterbalanced by GSH. The pathways competing for GSH are described to illustrate the events concurring to cause a depletion of endogenous GSH stocks. Drawing on evidence from literature that demonstrates the reduced levels of GSH in the main conditions clinically associated with severe disease, we highlight the relevance of restoring GSH levels in the attempt to protect the most vulnerable subjects from severe symptoms of COVID-19. Finally, we discuss the current data about the feasibility of increasing GSH levels, which could be used to prevent and subdue the disease. Full article
(This article belongs to the Special Issue ROS and COVID)
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