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Antioxidants
Special Issues
Reactive Sulfur Species in Oxidative Stress
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Reactive Sulfur Species in Oxidative 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 (15 January 2023) | Viewed by 3576

Special Issue Editors

Prof. Dr. Mark G. Clemens

E-Mail Website
Guest Editor
Center for Biomedical Science and Engineering, University of North Carolina at Charlotte, Charlotte, NC 28223, USA
Interests: nitric oxide; ischemia/reperfusion; inflammation; DNA damage/repair; hydrogen sulfide; liver; microcirculation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Adrian T. Press

E-Mail Website
Guest Editor
Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Friedrich-Schiller-University, Am Klinikum 1, 07747 Jena, Germany
Interests: infection; stress responses; liver, organ crosstalk; tissue organization; tissue remodeling; nano-medicine; drug delivery

Special Issue Information

Dear Colleagues,

Hydrogen sulfide (H2S) is now well recognized as the third important biological gaseous mediator. However, the importance of other reactive sulfur species (RSSs), most prominently H2S and its metabolites, is now being realized. H2S can be metabolized both enzymatically and non-enzymatically to other reactive sulfur species (including bound sulfane sulfur such as persulfide and thiosulphates, acid-labile sulfide, and bound thiols such as protein thiols). These RSSs control oxidative stress through chemical interactions, thiol protein regulation, and modification of bioenergetics of mitochondrial function. RSSs’ unique chemical properties have only recently been recognized, and biological concepts on RSSs involving cellular stress responses, protein biosynthesis, barrier function, and mitochondrial bioenergetics are just emerging. The Special Issue, “Reactive Sulfur Species in Oxidative Stress”, will provide a forum for publishing articles related to this timely and important topic.

Both review articles and original research articles within this area of research are welcome for submission in response to this SI. We will also send invitations to active researchers in this area.

Prof. Dr. Mark G. Clemens
Prof. Dr. Adrian T. Press
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

  • oxidative stress
  • cellular and tissue stress responses
  • reactive sulfur species
  • inflammation
  • damage control
  • thiosulfate

Published Papers (2 papers)

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Research

15 pages, 609 KiB  
Article
Contribution of Physical Activity to the Oxidative and Antioxidant Potential in 60–65-Year-Old Seniors
by Bartłomiej K. Sołtysik, Kamil Karolczak, Tomasz Kostka, Serena S. Stephenson, Cezary Watala and Joanna Kostka
Antioxidants 2023, 12(6), 1200; https://doi.org/10.3390/antiox12061200 - 31 May 2023
Viewed by 1078
Abstract
Both acute exercise and regular physical activity (PA) are directly related to the redox system. However, at present, there are data suggesting both positive and negative relationships between the PA and oxidation. In addition, there is a limited number of publications differentiating the [...] Read more.
Both acute exercise and regular physical activity (PA) are directly related to the redox system. However, at present, there are data suggesting both positive and negative relationships between the PA and oxidation. In addition, there is a limited number of publications differentiating the relationships between PA and numerous markers of plasma and platelets targets for the oxidative stress. In this study, in a population of 300 participants from central Poland (covering the age range between 60 and 65 years), PA was assessed as regards energy expenditure (PA-EE) and health-related behaviors (PA-HRB). Total antioxidant potential (TAS), total oxidative stress (TOS) and several other markers of an oxidative stress, monitored in platelet and plasma lipids and proteins, were then determined. The association of PA with oxidative stress was determined taking into the account basic confounders, such as age, sex and the set of the relevant cardiometabolic factors. In simple correlations, platelet lipid peroxides, free thiol and amino groups of platelet proteins, as well as the generation of superoxide anion radical, were inversely related with PA-EE. In multivariate analyses, apart from other cardiometabolic factors, a significant positive impact of PA-HRB was revealed for TOS (inverse relationship), while in the case of PA-EE, the effect was found to be positive (inverse association) for lipid peroxides and superoxide anion but negative (lower concentration) for free thiol and free amino groups in platelets proteins. Therefore, the impact of PA may be different on oxidative stress markers in platelets as compared to plasma proteins and also dissimilar on platelet lipids and proteins. These associations are more visible for platelets than plasma markers. For lipid oxidation, PA seems to have protective effect. In the case of platelets proteins, PA tends to act as pro-oxidative factor. Full article
(This article belongs to the Special Issue Reactive Sulfur Species in Oxidative Stress)
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17 pages, 3091 KiB  
Article
TNF-α-Mediated Endothelial Cell Apoptosis Is Rescued by Hydrogen Sulfide
by Lorena Diaz Sanchez, Lissette Sanchez-Aranguren, Keqing Wang, Corinne M. Spickett, Helen R. Griffiths and Irundika H. K. Dias
Antioxidants 2023, 12(3), 734; https://doi.org/10.3390/antiox12030734 - 16 Mar 2023
Cited by 5 | Viewed by 1861
Abstract
Endothelial dysfunction is implicated in the development and aggravation of cardiovascular complications. Among the endothelium-released vasoactive factors, hydrogen sulfide (H2S) has been investigated for its beneficial effects on the vasculature through anti-inflammatory and redox-modulating regulatory mechanisms. Reduced H2S bioavailability [...] Read more.
Endothelial dysfunction is implicated in the development and aggravation of cardiovascular complications. Among the endothelium-released vasoactive factors, hydrogen sulfide (H2S) has been investigated for its beneficial effects on the vasculature through anti-inflammatory and redox-modulating regulatory mechanisms. Reduced H2S bioavailability is reported in chronic diseases such as cardiovascular disease, diabetes, atherosclerosis and preeclampsia, suggesting the value of investigating mechanisms, by which H2S acts as a vasoprotective gasotransmitter. We explored whether the protective effects of H2S were linked to the mitochondrial health of endothelial cells and the mechanisms by which H2S rescues apoptosis. Here, we demonstrate that endothelial dysfunction induced by TNF-α increased endothelial oxidative stress and induced apoptosis via mitochondrial cytochrome c release and caspase activation over 24 h. TNF-α also affected mitochondrial morphology and altered the mitochondrial network. Post-treatment with the slow-releasing H2S donor, GYY4137, alleviated oxidising redox state, decreased pro-caspase 3 activity, and prevented endothelial apoptosis caused by TNF-α alone. In addition, exogenous GYY4137 enhanced S-sulfhydration of pro-caspase 3 and improved mitochondrial health in TNF-α exposed cells. These data provide new insights into molecular mechanisms for cytoprotective effects of H2S via the mitochondrial-driven pathway. Full article
(This article belongs to the Special Issue Reactive Sulfur Species in Oxidative Stress)
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