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Antioxidants
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Protein Oxidative Modification in Brain function, Brain Ageing and Neurological...
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Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases

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 January 2024) | Viewed by 6828

Special Issue Editors

Dr. Mattéa J. Finelli

E-Mail Website
Guest Editor
Biodiscovery Institute, University Park, Nottingham NG7 2RD, UK
Interests: neurodegenerative disease; oxidative stress; nitrosative stress; proteomics; metabolomics; stem-cell derived cellular models; neurosciences
Dr. Andreia N. Carvalho

E-Mail Website
Guest Editor
Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisboa, Portugal
Interests: mitochondria; mitochondrial dysfunction; oxidative stress; neurodegenerative disease; neurosciences

Special Issue Information

Dear Colleagues,

Reactive oxygen and nitrogen species (RONS) are molecules produced by the cellular energy metabolism, which drive the oxidoreduction (redox)-mediated signalling of the cells. Redox signalling plays an important role in the homeostatic control of several molecular pathways and in cell function, particularly changes in the redox status of Cysteine and other amino acid residues of proteins, which are extremely susceptible to reversible and irreversible oxidation by RONS. These changes can lead to redox-post-translational modifications (redox-PTMs) in proteins, which can directly affect protein structure, activity and function, ultimately impacting a multitude of biological functions.

Mitochondrial dysfunction and excessive RONS levels can give rise to oxidative and nitrosative stresses, and aberrant redox-PTMs (i.e., redox PTMs on lowly-reactive residues, and/or the addition of excessiveor irreversible redox-PTMs that may have oxidative damaging effects on proteins). Oxidative and nitrosative stresses and aberrant redox-PTMs are well-established contributors to a plethora of diseases, including neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and motor neuron diseases; however, the underlying mechanisms are not fully understood.

In this Special Issue, we invite original research articles and review articles related to the roles of the redox-PTMs-mediated signalling in modulating protein structure and activity, and brain function in health, ageing and neurological conditions.

We welcome studies exploring the mechanisms underlying the redox signalling mediated by redox-PTMs in the brain, as well as the therapeutic potential of modulating redox signalling and/or redox-PTMs in cells to treat neurological diseases (e.g., using small molecules or compounds). Manuscripts presenting new methods to study redox signalling mediated by redox-PTMs at the cellular and/or molecular levels (e.g., proteomics, RONS probes, etc) will also be considered.

This Special Issue aims to provide an overview of the field of redox biology and highlight the latest developments in the field, with a particular focus on redox signalling mediated by redox-PTMs of proteins and its role in the mammalian nervous system.

Dr. Mattéa J. Finelli
Dr. Andreia N. Carvalho
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

  • protein oxidative modifications
  • post-translational modifications
  • S-glutathionylation
  • S-nitrosylation/S-nitrosation
  • persulfidation
  • redox signalling
  • oxidative and nitrosative stresses
  • cysteine oxidation
  • antioxidants
  • redox-based pharmacological/therapeutic approaches
  • mitochondrial dysfunction
  • mitochondria-targeted molecules
  • brain function and ageing
  • neurological/neurodegenerative diseases
  • proteomics

Published Papers (4 papers)

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Research

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20 pages, 3877 KiB  
Article
Influence of Redox and Dopamine Regulation in Cocaine-Induced Phenotypes Using Drosophila
by Ana Filošević Vujnović, Marko Rubinić, Ivona Starčević and Rozi Andretić Waldowski
Antioxidants 2023, 12(4), 933; https://doi.org/10.3390/antiox12040933 - 14 Apr 2023
Cited by 2 | Viewed by 1730
Abstract
Reactive Oxidative Species (ROS) are produced during cellular metabolism and their amount is finely regulated because of negative consequences that ROS accumulation has on cellular functioning and survival. However, ROS play an important role in maintaining a healthy brain by participating in cellular [...] Read more.
Reactive Oxidative Species (ROS) are produced during cellular metabolism and their amount is finely regulated because of negative consequences that ROS accumulation has on cellular functioning and survival. However, ROS play an important role in maintaining a healthy brain by participating in cellular signaling and regulating neuronal plasticity, which led to a shift in our understanding of ROS from being solely detrimental to having a more complex role in the brain. Here we use Drosophila melanogaster to investigate the influence of ROS on behavioral phenotypes induced by single or double exposure to volatilized cocaine (vCOC), sensitivity and locomotor sensitization (LS). Sensitivity and LS depend on glutathione antioxidant defense. Catalase activity and hydrogen peroxide (H2O2) accumulation play a minor role, but their presence is necessary in dopaminergic and serotonergic neurons for LS. Feeding flies the antioxidant quercetin completely abolishes LS confirming the permissive role of H2O2 in the development of LS. This can only partially be rescued by co-feeding H2O2 or the dopamine precursor 3,4-dihydroxy-L-phenylalanine (L-DA) showing coordinate and similar contribution of dopamine and H2O2. Genetic versatility of Drosophila can be used as a tool for more precise dissection of temporal, spatial and transcriptional events that regulate behaviors induced by vCOC. Full article
(This article belongs to the Special Issue Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases)
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Review

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36 pages, 5451 KiB  
Review
A Combinational Therapy for Preventing and Delaying the Onset of Alzheimer’s Disease: A Focus on Probiotic and Vitamin Co-Supplementation
by Omme Fatema Sultana, Raksa Andalib Hia and P. Hemachandra Reddy
Antioxidants 2024, 13(2), 202; https://doi.org/10.3390/antiox13020202 - 05 Feb 2024
Viewed by 1682
Abstract
Alzheimer’s disease is a progressive neurodegenerative disorder with a complex etiology, and effective interventions to prevent or delay its onset remain a global health challenge. In recent years, there has been growing interest in the potential role of probiotic and vitamin supplementation as [...] Read more.
Alzheimer’s disease is a progressive neurodegenerative disorder with a complex etiology, and effective interventions to prevent or delay its onset remain a global health challenge. In recent years, there has been growing interest in the potential role of probiotic and vitamin supplementation as complementary strategies for Alzheimer’s disease prevention. This review paper explores the current scientific literature on the use of probiotics and vitamins, particularly vitamin A, D, E, K, and B-complex vitamins, in the context of Alzheimer’s disease prevention and management. We delve into the mechanisms through which probiotics may modulate gut–brain interactions and neuroinflammation while vitamins play crucial roles in neuronal health and cognitive function. The paper also examines the collective impact of this combinational therapy on reducing the risk factors associated with Alzheimer’s disease, such as oxidative stress, inflammation, and gut dysbiosis. By providing a comprehensive overview of the existing evidence and potential mechanisms, this review aims to shed light on the promise of probiotic and vitamin co-supplementation as a multifaceted approach to combat Alzheimer’s disease, offering insights into possible avenues for future research and clinical application. Full article
(This article belongs to the Special Issue Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases)
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15 pages, 1809 KiB  
Review
Regulation of Ras Signaling by S-Nitrosylation
by Sónia Simão, Rafaela Ribeiro Agostinho, Antonio Martínez-Ruiz and Inês Maria Araújo
Antioxidants 2023, 12(8), 1562; https://doi.org/10.3390/antiox12081562 - 04 Aug 2023
Cited by 2 | Viewed by 1173
Abstract
Ras are a family of small GTPases that function as signal transduction mediators and are involved in cell proliferation, migration, differentiation and survival. The significance of Ras is further evidenced by the fact that Ras genes are among the most mutated oncogenes in [...] Read more.
Ras are a family of small GTPases that function as signal transduction mediators and are involved in cell proliferation, migration, differentiation and survival. The significance of Ras is further evidenced by the fact that Ras genes are among the most mutated oncogenes in different types of cancers. After translation, Ras proteins can be targets of post-translational modifications (PTM), which can alter the intracellular dynamics of the protein. In this review, we will focus on how S-nitrosylation of Ras affects the way these proteins interact with membranes, its cellular localization, and its activity. S-Nitrosylation occurs when a nitrosyl moiety of nitric oxide (NO) is covalently attached to a thiol group of a cysteine residue in a target protein. In Ras, the conserved Cys118 is the most surface-exposed Cys and the preferable residue for NO action, leading to the initiation of transduction events. Ras transduces the mitogen-activated protein kinases (MAPK), the phosphoinositide-3 kinase (PI3K) and the RalGEF cellular pathways. S-Nitrosylation of elements of the RalGEF cascade remains to be identified. On the contrary, it is well established that several components of the MAPK and PI3K pathways, as well as different proteins associated with these cascades, can be modified by S-nitrosylation. Overall, this review presents a better understanding of Ras S-nitrosylation, increasing the knowledge on the dynamics of these proteins in the presence of NO and the underlying implications in cellular signaling. Full article
(This article belongs to the Special Issue Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases)
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16 pages, 1023 KiB  
Review
Oxidative Stress in Obstructive Sleep Apnea Syndrome: Putative Pathways to Hearing System Impairment
by Pierluigi Mastino, Davide Rosati, Giulia de Soccio, Martina Romeo, Daniele Pentangelo, Stefano Venarubea, Marco Fiore, Piero Giuseppe Meliante, Carla Petrella, Christian Barbato and Antonio Minni
Antioxidants 2023, 12(7), 1430; https://doi.org/10.3390/antiox12071430 - 15 Jul 2023
Cited by 2 | Viewed by 1501
Abstract
Introduction: OSAS is a disease that affects 2% of men and 4% of women of middle age. It is a major health public problem because untreated OSAS could lead to cardiovascular, metabolic, and cerebrovascular complications. The more accepted theory relates to oxidative stress [...] Read more.
Introduction: OSAS is a disease that affects 2% of men and 4% of women of middle age. It is a major health public problem because untreated OSAS could lead to cardiovascular, metabolic, and cerebrovascular complications. The more accepted theory relates to oxidative stress due to intermittent hypoxia, which leads, after an intense inflammatory response through multiple pathways, to endothelial damage. The objective of this study is to demonstrate a correlation between OSAS and hearing loss, the effect of the CPAP on hearing function, and if oxidative stress is also involved in the damaging of the hearing system. Methods: A review of the literature has been executed. Eight articles have been found, where seven were about the correlation between OSAS and the hearing system, and only one was about the CPAP effects. It is noted that two of the eight articles explored the theory of oxidative stress due to intermittent hypoxia. Results: All studies showed a significant correlation between OSAS and hearing function (p < 0.05).Conclusions: Untreated OSAS affects the hearing system at multiple levels. Oxidative stress due to intermittent hypoxia is the main pathogenetic mechanism of damage. CPAP has no effects (positive or negative) on hearing function. More studies are needed, with the evaluation of extended high frequencies, the execution of vocal audiometry in noisy environments, and the evaluation of potential biomarkers due to oxidative stress. Full article
(This article belongs to the Special Issue Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases)
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