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Antioxidants
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Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021
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Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021

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 (31 October 2021) | Viewed by 30190

Special Issue Editors

Prof. Dr. Anna Maria Fratta Pasini

E-Mail Website
Guest Editor
Department of Medicine, Section of Internal Medicine, University of Verona, 37134 Verona, Italy
Interests: oxidative stress and gene expression of antioxidant signaling pathways in chronic
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Luciano Cominacini

E-Mail Website
Guest Editor
Department of Medicine, Section of Internal Medicine, University of Verona, 37134 Verona, Italy
Interests: oxidative stress in physiopathology and therapy of atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) is causing the global coronavirus disease 2019 (COVID-19) pandemic. Oxidative stress (OS) has recently been suggested to play a key role in the pathogenesis of COVID-19 infection. SARS-CoV2-induced OS may be generated by different mechanisms. OS in turn may contribute to the initiation and progression of inflammation of type 2 alveolar epithelial and other kinds of cells often resulting in the death of these cells by apoptosis and pyroptosis. While it is likely that tissue damage caused by SARS-CoV-2 infection is the result of multifactorial mechanisms, very recent results indicate that OS may contribute to triggering the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, a component of the innate immune system that functions as a pattern recognition receptor that recognizes pathogen-associated molecular patterns. While it is likely that other pathological pathways co-participate in NLRP3 activation, NLRP3 inflammasome activation by reactive oxygen species (ROS) is induced through nuclear factor-kB (NF-kB) and thioredoxin interacting/inhibiting protein. OS also triggers NF-kB activation which, in turn, induces NLRP3, pro-interleukin (IL)-18, and pro-IL-1 expression, increasing the activation of NLRP3 inflammasome activity and pro-caspase-1 autocleavage that regulates IL-1b generation. It is known that the majority of respiratory viruses, including SARS-CoV-2, cause a multifactorial dysregulation of ROS generation. However, while exposure to many pro-oxidants usually induces Nrf2 activation and upregulation of antioxidant-related element (ARE) expression, respiratory viral infections often inhibit Nrf2 and/or activate NF-kB pathways resulting in inflammation and oxidative injury. Very interestingly the Nrf2 pathway has been shown to be suppressed in lung biopsies of patients affected by severe SARS-CoV-2. Pharmacological Nrf2 inducers have been reported to inhibit the replication of SARS-CoV-2, the inflammatory response, and the expression of transmembrane protease serine 2, a protease that favors SARS-CoV-2 entry into the host cells through the ACE2 receptor.

Contributions to this Special Issue may cover all research aspects related, but not limited to, studies evaluating:

  • OS evaluation in patients affected by SARS-CoV-2 and/or other respiratory viruses
  • Nrf2/ARE pathway status in patients with SARS-CoV-2 infection
  • Reciprocal crosstalk between Nrf2 and NF-kB pathways in SARS-CoV-2 infection
  • Mechanisms involved in SARS-CoV-2 ROS generation
  • Relationship between OS and inflammasome activation in SARS-CoV-2 infection
  • Possible role of redox-modulating agents in the treatment of SARS-CoV-2 infection
  • Possible role of Nrf2 inducers in the treatment of SARS-CoV-2 infection 

Dr. Anna Maria Fratta Pasini
Prof. Dr. Luciano Cominacini
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

  • Covid 19
  • SARS-CoV-2
  • Oxidative stress
  • Inflammation
  • Inflammasomes
  • Nrf2
  • NF-kB
  • ACE2
  • TMPRSS2
  • Cytokine storm

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

4 pages, 204 KiB  
Editorial
Effect of Antioxidant Therapy on Oxidative Stress In Vivo 2021
by Anna Maria Fratta Pasini and Luciano Cominacini
Antioxidants 2022, 11(3), 448; https://doi.org/10.3390/antiox11030448 - 24 Feb 2022
Cited by 2 | Viewed by 1414
Abstract
Oxidative stress (OS) is an imbalance between the formation of reactive oxygen and nitrogen species and antioxidant defenses [...] Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)

Research

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19 pages, 11207 KiB  
Article
Liposomal Glutathione Helps to Mitigate Mycobacterium tuberculosis Infection in the Lungs
by Nala Kachour, Abrianna Beever, James Owens, Ruoqiong Cao, Afsal Kolloli, Ranjeet Kumar, Kayvan Sasaninia, Charles Vaughn, Mohkam Singh, Edward Truong, Christopher Khatchadourian, Christina Sisliyan, Klara Zakery, Wael Khamas, Selvakumar Subbian and Vishwanath Venketaraman
Antioxidants 2022, 11(4), 673; https://doi.org/10.3390/antiox11040673 - 30 Mar 2022
Cited by 7 | Viewed by 3271
Abstract
Mycobacterium tuberculosis (M. tb), the causative agent of tuberculosis (TB), is responsible for causing significant morbidity and mortality, especially among individuals with compromised immune systems. We have previously shown that the supplementation of liposomal glutathione (L-GSH) reduces M. tb viability and [...] Read more.
Mycobacterium tuberculosis (M. tb), the causative agent of tuberculosis (TB), is responsible for causing significant morbidity and mortality, especially among individuals with compromised immune systems. We have previously shown that the supplementation of liposomal glutathione (L-GSH) reduces M. tb viability and enhances a Th-1 cytokine response, promoting granuloma formation in human peripheral blood mononuclear cells in vitro. However, the effects of L-GSH supplementation in modulating the immune responses in the lungs during an active M. tb infection have yet to be explored. In this article, we report the effects of L-GSH supplementation during an active M. tb infection in a mouse model of pulmonary infection. We determine the total GSH levels, malondialdehyde (MDA) levels, cytokine profiles, granuloma formation, and M. tb burden in untreated and L-GSH-treated mice over time. In 40 mM L-GSH-supplemented mice, an increase in the total GSH levels was observed in the lungs. When compared to untreated mice, the treatment of M. tb-infected mice with 40 mM and 80 mM L-GSH resulted in a reduction in MDA levels in the lungs. L-GSH treatment also resulted in a significant increase in the levels of IL-12, IFN-γ, IL-2, IL-17, and TNF-α in the lungs, while down-regulating the production of IL-6, IL-10, and TGF-β in the lungs. A reduction in M. tb survival along with a decrease in granuloma size in the lungs of M. tb-infected mice was observed after L-GSH treatment. Our results show that the supplementation of mice with L-GSH led to increased levels of total GSH, which is associated with reduced oxidative stress, increased levels of granuloma-promoting cytokines, and decreased M. tb burden in the lung. These results illustrate how GSH can help mitigate M. tb infection and provide an insight into future therapeutic interventions. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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22 pages, 7472 KiB  
Article
The Impact of Melatonin Supplementation and NLRP3 Inflammasome Deletion on Age-Accompanied Cardiac Damage
by Ramy K. A. Sayed, Marisol Fernández-Ortiz, Ibtissem Rahim, José Fernández-Martínez, Paula Aranda-Martínez, Iryna Rusanova, Laura Martínez-Ruiz, Reem M. Alsaadawy, Germaine Escames and Darío Acuña-Castroviejo
Antioxidants 2021, 10(8), 1269; https://doi.org/10.3390/antiox10081269 - 10 Aug 2021
Cited by 7 | Viewed by 4177
Abstract
To investigate the role of NLRP3 inflammasome in cardiac aging, we evaluate here morphological and ultrastructural age-related changes of cardiac muscles fibers in wild-type and NLRP3-knockout mice, as well as studying the beneficial effect of melatonin therapy. The results clarified the beginning of [...] Read more.
To investigate the role of NLRP3 inflammasome in cardiac aging, we evaluate here morphological and ultrastructural age-related changes of cardiac muscles fibers in wild-type and NLRP3-knockout mice, as well as studying the beneficial effect of melatonin therapy. The results clarified the beginning of the cardiac sarcopenia at the age of 12 months, with hypertrophy of cardiac myocytes, increased expression of β-MHC, appearance of small necrotic fibers, decline of cadiomyocyte number, destruction of mitochondrial cristae, appearance of small-sized residual bodies, and increased apoptotic nuclei ratio. These changes were progressed in the cardiac myocytes of 24 old mice, accompanied by excessive collagen deposition, higher expressions of IL-1α, IL-6, and TNFα, complete mitochondrial vacuolation and damage, myofibrils disorganization, multivesicular bodies formation, and nuclear fragmentation. Interestingly, cardiac myocytes of NLRP3−/− mice showed less detectable age-related changes compared with WT mice. Oral melatonin therapy preserved the normal cardiomyocytes structure, restored cardiomyocytes number, and reduced β-MHC expression of cardiac hypertrophy. In addition, melatonin recovered mitochondrial architecture, reduced apoptosis and multivesicular bodies’ formation, and decreased expressions of β-MHC, IL-1α, and IL-6. Fewer cardiac sarcopenic changes and highly remarkable protective effects of melatonin treatment detected in aged cardiomyocytes of NLRP3−/− mice compared with aged WT animals, confirming implication of the NLRP3 inflammasome in cardiac aging. Thus, NLRP3 suppression and melatonin therapy may be therapeutic approaches for age-related cardiac sarcopenia. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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18 pages, 3769 KiB  
Article
Inhibition of Oxidative Stress and ALOX12 and NF-κB Pathways Contribute to the Protective Effect of Baicalein on Carbon Tetrachloride-Induced Acute Liver Injury
by Chongshan Dai, Hui Li, Yang Wang, Shusheng Tang, Tony Velkov and Jianzhong Shen
Antioxidants 2021, 10(6), 976; https://doi.org/10.3390/antiox10060976 - 18 Jun 2021
Cited by 57 | Viewed by 4716
Abstract
This study investigates the protective effect of baicalein on carbon tetrachloride (CCl4)-induced acute liver injury and the underlying molecular mechanisms. Mice were orally administrated baicalein at 25 and 100 mg/kg/day for 7 consecutive days or ferrostatin-1 (Fer-1) at 10 mg/kg was [...] Read more.
This study investigates the protective effect of baicalein on carbon tetrachloride (CCl4)-induced acute liver injury and the underlying molecular mechanisms. Mice were orally administrated baicalein at 25 and 100 mg/kg/day for 7 consecutive days or ferrostatin-1 (Fer-1) at 10 mg/kg was i.p. injected in mice at 2 and 24 h prior to CCl4 injection or the vehicle. Our results showed that baicalein or Fer-1 supplementation significantly attenuated CCl4 exposure-induced elevations of serum alanine aminotransferase and aspartate aminotransferase, and malondialdehyde levels in the liver tissues and unregulated glutathione levels. Baicalein treatment inhibited the nuclear factor kappa-B (NF-κB) pathway, activated the erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway in liver tissues, and markedly improved CCl4-induced apoptosis, inflammation and ferroptosis in liver tissues exposed with CCl4. In vitro, baicalein treatment improved CCl4 -induced decreases of cell viabilities and knockdown of Nrf2 and arachidonate 12-lipoxygenase (ALOX12) genes partly abolished the protective effect of baicalein on CCl4 -induced cytotoxicity in HepG2 cells. In conclusion, our results reveal that baicalein supplementation ameliorates CCl4-induced acute liver injury in mice by upregulating the antioxidant defense pathways and downregulating oxidative stress, apoptosis, inflammation and ferroptosis, which involved the activation of Nrf2 pathway and the inhibition of ALOX12 and NF-κB pathways. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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20 pages, 4206 KiB  
Article
Oxidative Stress and Its Consequences in the Blood of Rats Irradiated with UV: Protective Effect of Cannabidiol
by Michał Biernacki, Małgorzata Michalina Brzóska, Agnieszka Markowska, Małgorzata Gałażyn-Sidorczuk, Bogdan Cylwik, Agnieszka Gęgotek and Elżbieta Skrzydlewska
Antioxidants 2021, 10(6), 821; https://doi.org/10.3390/antiox10060821 - 21 May 2021
Cited by 16 | Viewed by 3600
Abstract
UVA/UVB radiation disturbs the redox balance of skin cells, and metabolic consequences can be transferred into the blood and internal tissues, especially after chronic skin exposure to UV radiation. Therefore, the aim of this study was to evaluate the effect of cannabidiol (CBD), [...] Read more.
UVA/UVB radiation disturbs the redox balance of skin cells, and metabolic consequences can be transferred into the blood and internal tissues, especially after chronic skin exposure to UV radiation. Therefore, the aim of this study was to evaluate the effect of cannabidiol (CBD), an antioxidant and anti-inflammatory phytocannabinoid, on oxidative stress and its consequences in the blood of nude rats whose skin was exposed to UVA/UVB radiation for 4 weeks. It was shown that CBD penetrated the blood and in UVB-irradiated rats was preferentially located in the membranes of polymorphonuclear leukocytes, which promoted reduction of ROS generation and up-regulation of antioxidant ability by increasing the activity of glutathione reductase and thioredoxin reductase, while the level of reduced glutathione decreased by UV radiation. Consequently, reduction in UV-induced lipid peroxidation, assessed as 4-hydroxynonenal (4-HNE) and 8-isoprostane (8-isoPGF2α) as well as protein modifications, estimated as 4-HNE-protein adducts and protein carbonyl groups, was observed. CBD, by countering the UV-induced down-regulation of 2-arachidonylglycerol, promoted its antioxidant/anti-inflammatory effects by reducing CB1 and increasing PPARγ receptor activation and consequently ROS and TNF-α down-regulation. The results suggest that CBD applied topically to the skin minimizes redox changes not only at the skin level, but also at the systemic level. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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Review

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30 pages, 3179 KiB  
Review
The Multiple Effects of Vitamin D against Chronic Diseases: From Reduction of Lipid Peroxidation to Updated Evidence from Clinical Studies
by Massimiliano Berretta, Vincenzo Quagliariello, Alessia Bignucolo, Sergio Facchini, Nicola Maurea, Raffaele Di Francia, Francesco Fiorica, Saman Sharifi, Silvia Bressan, Sara N. Richter, Valentina Camozzi, Luca Rinaldi, Carla Scaroni and Monica Montopoli
Antioxidants 2022, 11(6), 1090; https://doi.org/10.3390/antiox11061090 - 30 May 2022
Cited by 18 | Viewed by 4664
Abstract
Background: Vitamin D exerts multiple beneficial effects in humans, including neuronal, immune, and bone homeostasis and the regulation of cardiovascular functions. Recent studies correlate vitamin D with cancer cell growth and survival, but meta-analyses on this topic are often not consistent. Methods: A [...] Read more.
Background: Vitamin D exerts multiple beneficial effects in humans, including neuronal, immune, and bone homeostasis and the regulation of cardiovascular functions. Recent studies correlate vitamin D with cancer cell growth and survival, but meta-analyses on this topic are often not consistent. Methods: A systematic search of the PubMed database and the Clinical Trial Register was performed to identify all potentially relevant English-language scientific papers containing original research articles on the effects of vitamin D on human health. Results: In this review, we analyzed the antioxidant and anti-inflammatory effects of vitamin D against acute and chronic diseases, focusing particularly on cancer, immune-related diseases, cardiomyophaties (including heart failure, cardiac arrhythmias, and atherosclerosis) and infectious diseases. Conclusions: Vitamin D significantly reduces the pro-oxidant systemic and tissue biomarkers involved in the development, progression, and recurrence of chronic cardiometabolic disease and cancer. The overall picture of this review provides the basis for new randomized controlled trials of oral vitamin D supplementation in patients with cancer and infectious, neurodegenerative, and cardiovascular diseases aimed at reducing risk factors for disease recurrence and improving quality of life. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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20 pages, 1634 KiB  
Review
Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
by Anna Maria Fratta Pasini, Chiara Stranieri, Domenico Girelli, Fabiana Busti and Luciano Cominacini
Antioxidants 2021, 10(11), 1677; https://doi.org/10.3390/antiox10111677 - 25 Oct 2021
Cited by 45 | Viewed by 7425
Abstract
Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent [...] Read more.
Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the cytoplasm of cystine, a precursor of glutathione (GSH) in exchange with glutamate and the consequent malfunction of GPX4. Ferroptosis is also promoted by intracellular iron overload and by the iron-dependent accumulation of polyunsaturated fatty acids (PUFA)-derived lipid peroxides. Since depletion of GSH, inactivation of GPX4, altered iron metabolism, and upregulation of PUFA peroxidation by reactive oxygen species are peculiar signs of COVID-19, there is the possibility that SARS-CoV-2 may trigger ferroptosis in the cells of multiple organs, thus contributing to multiorgan damage. Here, we review the molecular mechanisms of ferroptosis and its possible relationship with SARS-CoV-2 infection and multiorgan damage. Finally, we analyze the potential interventions that may combat ferroptosis and, therefore, reduce multiorgan damage. Full article
(This article belongs to the Special Issue Effect of Antioxidant Therapy on Oxidative Stress in Vivo 2021)
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