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Antioxidants
Special Issues
Redox and Nitrosative Signaling and Stress
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Redox and Nitrosative Signaling and Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 31669

Special Issue Editor

Prof. Dr. Claudia Penna

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Guest Editor
Laboratory of Cardiovascular Physiology, Dipartimento di Scienze Cliniche e Biologiche, Università Degli Studi di Torino, Regione Gonzole 10, 10043 Orbassano, Italy
Interests: cardiovascular system; physiological endothelial functions; coronary circulation; metabolism; contractility; myocardial protection; endothelial cells; vitamins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Redox/nitrosative signaling levels intervene in many human physiological adaptations and in many pathophysiological processes, leading to diseases such as cancer, neurodegenerative disease, lung disease, cardiovascular diseases, and ischemia/reperfusion injury. Recently, redox approaches have also shown promise in enhancing the levels of tolerance to cardio-toxic anticancer drugs and protecting from or inhibiting the progression of these diseases. The main scope of the present Special Issue is to reach a broad audience of scientists working in the field of redox biomedicine. We encourage the submission of papers approaching the topic from different points of view and at different levels, from basic to translational research in several cardiovascular fields. 

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning redox and nitrosative signaling both in normal processes and diseased states. This research can include both in vitro and in vivo studies relating to any of the following topics, though not exclusively: regulation of antioxidant enzymes; redox dependent post-translational modifications of proteins; role of redox state in cell metabolism, cell cycle, epigenetic regulation, cellular stress, and disease. Studies on organ protection and organ toxicity are also welcome.

We look forward to your contribution.

Prof. Dr. Claudia Penna
Guest Editor

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 (7 papers)

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Editorial

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2 pages, 157 KiB  
Editorial
Redox and Nitrosative Signaling and Stress
by Claudia Penna
Antioxidants 2020, 9(12), 1237; https://doi.org/10.3390/antiox9121237 - 07 Dec 2020
Viewed by 1229
Abstract
In this Special Issue, redox/nitrosative signaling has been considered in several aspects of cardiosciences and oncology, namely cardioncology [...] Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)

Research

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16 pages, 2718 KiB  
Article
Placental Adaptive Changes to Protect Function and Decrease Oxidative Damage in Metabolically Healthy Maternal Obesity
by Celeste Santos-Rosendo, Fernando Bugatto, Alvaro González-Domínguez, Alfonso M. Lechuga-Sancho, Rosa Maria Mateos and Francisco Visiedo
Antioxidants 2020, 9(9), 794; https://doi.org/10.3390/antiox9090794 - 26 Aug 2020
Cited by 16 | Viewed by 3534
Abstract
Pregnancy-related disorders, including preeclampsia and gestational diabetes, are characterized by the presence of an adverse intrauterine milieu that may ultimately result in oxidative and nitrosative stress. This scenario may trigger uncontrolled production of reactive oxygen species (ROS) such as superoxide anion (O●− [...] Read more.
Pregnancy-related disorders, including preeclampsia and gestational diabetes, are characterized by the presence of an adverse intrauterine milieu that may ultimately result in oxidative and nitrosative stress. This scenario may trigger uncontrolled production of reactive oxygen species (ROS) such as superoxide anion (O●−) and reactive nitrogen species (RNS) such as nitric oxide (NO), along with an inactivation of antioxidant systems, which are associated with the occurrence of relevant changes in placental function through recognized redox post-translational modifications in key proteins. The general objective of this study was to assess the impact of a maternal obesogenic enviroment on the regulation of the placental nitroso-redox balance at the end of pregnancy. We measured oxidative damage markers—thiobarbituric acid-reacting substances (TBARS) and carbonyl groups (C=O) levels; nitrosative stress markers—inducible nitric oxide synthase, nitrosothiol groups, and nitrotyrosine residues levels; and the antioxidant biomarkers—catalase and superoxide dismutase (SOD) activity and expression, and total antioxidant capacity (TAC), in full-term placental villous from both pre-pregnancy normal weight and obese women, and with absence of metabolic complications throughout gestation. The results showed a decrease in C=O and TBARS levels in obese pregnancies. Although total SOD and catalase concentrations were shown to be increased, both activities were significantly downregulated in obese pregnancies, along with total antioxidant capacity. Inducible nitric oxide sintase levels were increased in the obese group compared to the lean group, accompanied by an increase in nitrotyrosine residues levels and lower levels of nitrosothiol groups in proteins such as ERK1/2. These findings reveal a reduction in oxidative damage, accompanied by a decline in antioxidant response, and an increase via NO-mediated nitrative stress in placental tissue from metabolically healthy pregnancies with obesity. All this plausibly points to a placental adaptation of the affected antioxidant response towards a NO-induced alternative pathway, through changes in the ROS/RNS balance, in order to reduce oxidative damage and preserve placental function in pregnancy. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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14 pages, 2959 KiB  
Article
Circuits Regulating Superoxide and Nitric Oxide Production and Neutralization in Different Cell Types: Expression of Participating Genes and Changes Induced by Ionizing Radiation
by Patryk Bil, Sylwia Ciesielska, Roman Jaksik and Joanna Rzeszowska-Wolny
Antioxidants 2020, 9(8), 701; https://doi.org/10.3390/antiox9080701 - 03 Aug 2020
Cited by 4 | Viewed by 3168
Abstract
Superoxide radicals, together with nitric oxide (NO), determine the oxidative status of cells, which use different pathways to control their levels in response to stressing conditions. Using gene expression data available in the Cancer Cell Line Encyclopedia and microarray results, we compared the [...] Read more.
Superoxide radicals, together with nitric oxide (NO), determine the oxidative status of cells, which use different pathways to control their levels in response to stressing conditions. Using gene expression data available in the Cancer Cell Line Encyclopedia and microarray results, we compared the expression of genes engaged in pathways controlling reactive oxygen species and NO production, neutralization, and changes in response to the exposure of cells to ionizing radiation (IR) in human cancer cell lines originating from different tissues. The expression of NADPH oxidases and NO synthases that participate in superoxide radical and NO production was low in all cell types. Superoxide dismutase, glutathione peroxidase, thioredoxin, and peroxiredoxins participating in radical neutralization showed high expression in nearly all cell types. Some enzymes that may indirectly influence superoxide radical and NO levels showed tissue-specific expression and differences in response to IR. Using fluorescence microscopy and specific dyes, we followed the levels and the distribution of superoxide and NO radicals in living melanoma cells at different times after exposure to IR. Directly after irradiation, we observed an increase of superoxide radicals and NO coexistent in the same subcellular locations, suggesting a switch of NO synthase to the production of superoxide radicals. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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15 pages, 3571 KiB  
Article
Dauricine Protects from LPS-Induced Bone Loss via the ROS/PP2A/NF-κB Axis in Osteoclasts
by Hyun-Jung Park, Malihatosadat Gholam Zadeh, Jae-Hee Suh and Hye-Seon Choi
Antioxidants 2020, 9(7), 588; https://doi.org/10.3390/antiox9070588 - 06 Jul 2020
Cited by 18 | Viewed by 3315
Abstract
Dauricine (DAC), an isoquinoline alkaloid, exhibits anti-inflammatory activity. We hypothesized that DAC may prevent the inflammatory bone loss induced by lipopolysaccharide (LPS). LPS-induced bone loss was decreased by DAC in female C57BL/6J mice as evaluated by micro-computerized tomography (μCT) analysis. In vivo tartrate-resistant [...] Read more.
Dauricine (DAC), an isoquinoline alkaloid, exhibits anti-inflammatory activity. We hypothesized that DAC may prevent the inflammatory bone loss induced by lipopolysaccharide (LPS). LPS-induced bone loss was decreased by DAC in female C57BL/6J mice as evaluated by micro-computerized tomography (μCT) analysis. In vivo tartrate-resistant acid phosphatase (TRAP) staining showed that the increased number of osteoclasts (OCs) in LPS-treated mice was attenuated by DAC, indicating that DAC exhibited bone sparing effects through acting on OCs. DAC also decreased the differentiation and activity of OCs after LPS stimulation in vitro. LPS-induced cytosolic reactive oxygen species (cROS) oxidized PP2A, a serine/threonine phosphatase, leading to the activation of IKKα/β, followed by the nuclear localization of p65. DAC decreased LPS-induced ROS, resulting in the recovery of the activity of PP2A by reducing its oxidized form. Consequently, DAC reduced the phosphorylation of IKKα/β to block the nuclear localization of p65, which decreased NF-κB activation. Taken together, DAC reduced the differentiation and activity of OCs by decreasing ROS via the ROS/PP2A/NF-κB axis, resulting in protection from LPS-induced bone loss. We have demonstrated that LPS-induced bone loss was inhibited by DAC via its action on OCs, implying the therapeutic potential of DAC against inflammatory bone loss. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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Review

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14 pages, 643 KiB  
Review
Squalene: More than a Step toward Sterols
by Marco Micera, Alfonso Botto, Federica Geddo, Susanna Antoniotti, Cinzia Margherita Bertea, Renzo Levi, Maria Pia Gallo and Giulia Querio
Antioxidants 2020, 9(8), 688; https://doi.org/10.3390/antiox9080688 - 02 Aug 2020
Cited by 57 | Viewed by 8152
Abstract
Squalene (SQ) is a natural triterpene widely distributed in nature. It is a metabolic intermediate of the sterol biosynthetic pathway and represents a possible target in different metabolic and oxidative stress-related disorders. Growing interest has been focused on SQ’s antioxidant properties, derived from [...] Read more.
Squalene (SQ) is a natural triterpene widely distributed in nature. It is a metabolic intermediate of the sterol biosynthetic pathway and represents a possible target in different metabolic and oxidative stress-related disorders. Growing interest has been focused on SQ’s antioxidant properties, derived from its chemical structure. Strong evidence provided by ex vivo models underline its scavenging activity towards free radicals, whereas only a few studies have highlighted its effect in cellular models of oxidative stress. Given the role of unbalanced free radicals in both the onset and progression of several cardiovascular diseases, an in depth evaluation of SQ’s contribution to antioxidant defense mechanisms could represent a strategic approach in dealing with these pathological conditions. At present experimental results overall show a double-edged sword role of squalene in cardiovascular diseases and its function has to be better elucidated in order to establish intervention lines focused on its features. This review aims to summarize current knowledge about endogenous and exogenous sources of SQ and to point out the controversial role of SQ in cardiovascular physiology. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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20 pages, 1038 KiB  
Review
Redox Imbalances in Ageing and Metabolic Alterations: Implications in Cancer and Cardiac Diseases. An Overview from the Working Group of Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology (SIC)
by Valentina Mercurio, Alessandra Cuomo, Christian Cadeddu Dessalvi, Martino Deidda, Daniela Di Lisi, Giuseppina Novo, Roberta Manganaro, Concetta Zito, Ciro Santoro, Pietro Ameri, Paolo Spallarossa, Eleonora Arboscello, Carlo Gabriele Tocchetti and Claudia Penna
Antioxidants 2020, 9(7), 641; https://doi.org/10.3390/antiox9070641 - 21 Jul 2020
Cited by 24 | Viewed by 3618
Abstract
Metabolic syndrome (MetS) is a well established risk factor for cardiovascular (CV) diseases. In addition, several studies indicate that MetS correlates with the increased risk of cancer in adults. The mechanisms linking MetS and cancer are not fully understood. Several risk factors involved [...] Read more.
Metabolic syndrome (MetS) is a well established risk factor for cardiovascular (CV) diseases. In addition, several studies indicate that MetS correlates with the increased risk of cancer in adults. The mechanisms linking MetS and cancer are not fully understood. Several risk factors involved in MetS are also cancer risk factors, such as the consumption of high calorie-food or high fat intake, low fibre intake, and sedentary lifestyle. Other common aspects of both cancer and MetS are oxidative stress and inflammation. In addition, some anticancer treatments can induce cardiotoxicity, including, for instance, left ventricular (LV) dysfunction and heart failure (HF), endothelial dysfunction and hypertension. In this review, we analyse several aspects of MetS, cancer and cardiotoxicity from anticancer drugs. In particular, we focus on oxidative stress in ageing, cancer and CV diseases, and we analyse the connections among CV risk factors, cancer and cardiotoxicity from anticancer drugs. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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14 pages, 1062 KiB  
Review
An Update on Mitochondrial Reactive Oxygen Species Production
by Ryan J. Mailloux
Antioxidants 2020, 9(6), 472; https://doi.org/10.3390/antiox9060472 - 02 Jun 2020
Cited by 126 | Viewed by 8092
Abstract
Mitochondria are quantifiably the most important sources of superoxide (O2●−) and hydrogen peroxide (H2O2) in mammalian cells. The overproduction of these molecules has been studied mostly in the contexts of the pathogenesis of human diseases and [...] Read more.
Mitochondria are quantifiably the most important sources of superoxide (O2●−) and hydrogen peroxide (H2O2) in mammalian cells. The overproduction of these molecules has been studied mostly in the contexts of the pathogenesis of human diseases and aging. However, controlled bursts in mitochondrial ROS production, most notably H2O2, also plays a vital role in the transmission of cellular information. Striking a balance between utilizing H2O2 in second messaging whilst avoiding its deleterious effects requires the use of sophisticated feedback control and H2O2 degrading mechanisms. Mitochondria are enriched with H2O2 degrading enzymes to desensitize redox signals. These organelles also use a series of negative feedback loops, such as proton leaks or protein S-glutathionylation, to inhibit H2O2 production. Understanding how mitochondria produce ROS is also important for comprehending how these organelles use H2O2 in eustress signaling. Indeed, twelve different enzymes associated with nutrient metabolism and oxidative phosphorylation (OXPHOS) can serve as important ROS sources. This includes several flavoproteins and respiratory complexes I-III. Progress in understanding how mitochondria generate H2O2 for signaling must also account for critical physiological factors that strongly influence ROS production, such as sex differences and genetic variances in genes encoding antioxidants and proteins involved in mitochondrial bioenergetics. In the present review, I provide an updated view on how mitochondria budget cellular H2O2 production. These discussions will focus on the potential addition of two acyl-CoA dehydrogenases to the list of ROS generators and the impact of important phenotypic and physiological factors such as tissue type, mouse strain, and sex on production by these individual sites. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling and Stress)
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