Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Thiol Redox Systems in Health and Disease
share announcement

Thiol Redox Systems in Health and Disease

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 July 2018) | Viewed by 12555

Special Issue Editor

Prof. Dr. Gethin J. McBean

E-Mail Website
Guest Editor
UCD School of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin 4, Ireland
Interests: mechanisms of action of antioxidants in the brain; particularly, the importance of sulfur-containing amino acids in thiol redox balance and antioxidant defence in astrocytes and microglial cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thiol redox homeostasis is essential for the growth and development of living organisms, and is particularly important in protecting cells and tissues from oxidative stress. However, it is increasingly recognized that changes in the oxidation state of protein thiols is a significant mechanism for regulation of physiological, as well as pathological function.

This Special Issue will publish original research papers and review articles on a range of topics that relate to thiol redox homeostasis under normal and pathological conditions in mammalian systems. For example, the cysteine/cystine and oxidised and reduced glutathione redox pairs; thioredoxin/thioredoxin reductases; glutaredoxins, peroxiredoxins; glutathionylation; metabolic pathways that contribute to thiol redox homeostasis; thiol redox-sensitive enzymes; methods of detection of changes in thiol redox balance in mammalian cells; changes in thiol redox status in response to oxidative stress; the association between thiol redox status and disease in animals and humans.

Prof. Dr. Gethin J. McBean
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 (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

17 pages, 1663 KiB  
Review
The Role of Cystinosin in the Intermediary Thiol Metabolism and Redox Homeostasis in Kidney Proximal Tubular Cells
by Rodolfo Sumayao, Jr., Philip Newsholme and Tara McMorrow
Antioxidants 2018, 7(12), 179; https://doi.org/10.3390/antiox7120179 - 03 Dec 2018
Cited by 16 | Viewed by 4579
Abstract
Cystinosin is a lysosomal transmembrane protein which facilitates transport of the disulphide amino acid cystine (CySS) from the lysosomes of the cell. This protein is encoded by the CTNS gene which is defective in the lysosomal storage disorder, cystinosis. Because of the apparent [...] Read more.
Cystinosin is a lysosomal transmembrane protein which facilitates transport of the disulphide amino acid cystine (CySS) from the lysosomes of the cell. This protein is encoded by the CTNS gene which is defective in the lysosomal storage disorder, cystinosis. Because of the apparent involvement of cystinosin in the intermediary thiol metabolism, its discovery has fuelled investigations into its role in modulating cellular redox homeostasis. The kidney proximal tubular cells (PTCs) have become the focus of various studies on cystinosin since the protein is highly expressed in these cells and kidney proximal tubular transport dysfunction is the foremost clinical manifestation of cystinosis. The lysosomal CySS pool is a major source of cytosolic cysteine (Cys), the limiting amino acid for the synthesis of an important antioxidant glutathione (GSH) via the γ-glutamyl cycle. Therefore, loss of cystinosin function is presumed to lead to cytosolic deficit of Cys which may impair GSH synthesis. However, studies using in vitro models lacking cystinosin yielded inconsistent results and failed to establish the mechanistic role of cystinosin in modulating GSH synthesis and redox homeostasis. Because of the complexity of the metabolic micro- and macro-environment in vivo, using in vitro models alone may not be able to capture the complete sequence of biochemical and physiological events that occur as a consequence of loss of cystinosin function. The coexistence of pathways for the overall handling and disposition of GSH, the modulation of CTNS gene by intracellular redox status and the existence of a non-canonical isoform of cystinosin may constitute possible rescue mechanisms in vivo to remediate redox perturbations in renal PTCs. Importantly, the mitochondria seem to play a critical role in orchestrating redox imbalances initiated by cystinosin dysfunction. Non-invasive techniques such as in vivo magnetic resonance imaging with the aid of systems biology approaches may provide invaluable mechanistic insights into the role of cystinosin in the essential intermediary thiol metabolism and in the overall regulation cellular redox homeostasis. Full article
(This article belongs to the Special Issue Thiol Redox Systems in Health and Disease)
►▼ Show Figures

Figure 1

34 pages, 1709 KiB  
Review
The Plasma Membrane: A Platform for Intra- and Intercellular Redox Signaling
by Daniela E. Nordzieke and Iria Medraño-Fernandez
Antioxidants 2018, 7(11), 168; https://doi.org/10.3390/antiox7110168 - 20 Nov 2018
Cited by 60 | Viewed by 7453
Abstract
Membranes are of outmost importance to allow for specific signal transduction due to their ability to localize, amplify, and direct signals. However, due to the double-edged nature of reactive oxygen species (ROS)—toxic at high concentrations but essential signal molecules—subcellular localization of ROS-producing systems [...] Read more.
Membranes are of outmost importance to allow for specific signal transduction due to their ability to localize, amplify, and direct signals. However, due to the double-edged nature of reactive oxygen species (ROS)—toxic at high concentrations but essential signal molecules—subcellular localization of ROS-producing systems to the plasma membrane has been traditionally regarded as a protective strategy to defend cells from unwanted side-effects. Nevertheless, specialized regions, such as lipid rafts and caveolae, house and regulate the activated/inhibited states of important ROS-producing systems and concentrate redox targets, demonstrating that plasma membrane functions may go beyond acting as a securing lipid barrier. This is nicely evinced by nicotinamide adenine dinucleotide phosphate (NADPH)-oxidases (NOX), enzymes whose primary function is to generate ROS and which have been shown to reside in specific lipid compartments. In addition, membrane-inserted bidirectional H2O2-transporters modulate their conductance precisely during the passage of the molecules through the lipid bilayer, ensuring time-scaled delivery of the signal. This review aims to summarize current evidence supporting the role of the plasma membrane as an organizing center that serves as a platform for redox signal transmission, particularly NOX-driven, providing specificity at the same time that limits undesirable oxidative damage in case of malfunction. As an example of malfunction, we explore several pathological situations in which an inflammatory component is present, such as inflammatory bowel disease and neurodegenerative disorders, to illustrate how dysregulation of plasma-membrane-localized redox signaling impacts normal cell physiology. Full article
(This article belongs to the Special Issue Thiol Redox Systems in Health and Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop