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Antioxidants
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Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic...
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Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic Brain Injury

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 13537

Special Issue Editors

Prof. Dr. Barbara Tavazzi

E-Mail Website
Guest Editor
Departmental Faculty of Medicine and Surgery, UniCamillus-Saint Camillus International University of Health and Medical Sciences, via di Sant’Alessandro 8, 00131 Rome, Italy
Interests: neurodegenerative acute (traumatic brain injury) and chronic (multiple sclerosis) disorders; oxidative and nitrosative stresses; oxidation mechanisms; antioxidants; metabolomics; biochemical analytical techniques; lipid peroxidation products; dietary antioxidants; carotenoids; polyphenols; vitamin E; vitamin C; antioxidant activity/capacity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giacomo Lazzarino

E-Mail Website
Co-Guest Editor
UniCamillus—Saint Camillus International University of Health Sciences, Via di Sant’Alessandro 8, 00131 Rome, Italy
Interests: mitochondrial dysfunction; oxidative/nitrosative stress; neurodegenerations; multiple sclerosis; traumatic brain injury; metabolic cell reprogramming
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Angela Maria Amorini

E-Mail Website
Co-Guest Editor
Department of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Via Santa Sofia 87, 95125 Catania, Italy
Interests: neurodegenerative acute (traumatic brain injury) and chronic (multiple sclerosis) disorders; oxidative and nitrosative stresses; oxidation mechanisms
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Traumatic brain injury (TBI) remains one of the leading causes of morbidity and mortality amongst adults in Western countries. Despite advances in our knowledge of the complex pathophysiology of TBI, the underlying mechanisms are yet to be fully elucidated. This neurodegeneration consists of not only morphological damage but also a further, profound, hidden and somehow ‘invisible’ biochemical harm, initiated by the inertial forces acting on the brain tissue at the time of impact. These forces trigger a cascade of molecular events altering a plethora of cellular functions including ionic homeostasis, mitochondrial functions, energy metabolism, neurotransmission, signal transduction, protein folding, gene expression, and apoptosis. Various experimental studies have ultimately demonstrated that these and other changes are strictly related to severity of injury, in turn, related to the amount of the mechanical energy transferred at the time of impact, with mild TBI (mTBI) mostly causing spontaneously resolving changes, and with severe TBI (sTBI) mainly provoking permanent alterations of pivotal cerebral cell functions.

The shift of normal mitochondrial activity to pathological activity after TBI, lies in an initial functional-to-dysfunctional transition state causing, in turn, the activation of dangerous pathological reactions, potentially leading to definitive, irreversible mitochondrial damage. Reversing mitochondrial malfunctioning may be crucial to avoiding irreversible processes being triggered, such as apoptosis, thus, preventing the physiology-to-pathology shift.

In TBI, dysfunctional mitochondria are involved in the generation of oxidative/nitrosative stress, caused by the excess production of reactive oxygen and nitrogen species (ROS and RNS, respectively), as well as in the induction of apoptosis.

This Special Issue will publish original research papers and reviews that investigate the implications of mitochondrial dysfunction, oxidative stress, and dysmetabolic conditions after a TBI, as well as in preclinical and clinical studies.

We cordially invite scientists involved in base research to submit their original research or review manuscripts to this Special Issue on “Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic Brain Injury”.

Original research reports and reviews will be published online in Antioxidants.

Prof. Dr. Barbara Tavazzi
Prof. Giacomo Lazzarino
Prof. Angela Maria Amorini
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

  • Traumatic brain injury
  • Mitochondrial dysfunction
  • Mitochondrial quality control
  • Oxidative and nitrosative stresses
  • Purines and pyrimidines metabolism
  • Metabolism of amino acids and amino compounds
  • Degrees of severity of TBI
  • Apoptosis
  • Brain imaging
  • Serum biomarkers
  • Secondary injury

Published Papers (3 papers)

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Research

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23 pages, 3391 KiB  
Article
Regulation of Phosphorylated State of NMDA Receptor by STEP61 Phosphatase after Mild-Traumatic Brain Injury: Role of Oxidative Stress
by Francisco J. Carvajal and Waldo Cerpa
Antioxidants 2021, 10(10), 1575; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10101575 - 05 Oct 2021
Cited by 10 | Viewed by 2445
Abstract
Traumatic Brain Injury (TBI) mediates neuronal death through several events involving many molecular pathways, including the glutamate-mediated excitotoxicity for excessive stimulation of N-methyl-D-aspartate receptors (NMDARs), producing activation of death signaling pathways. However, the contribution of NMDARs (distribution and signaling-associated to the distribution) remains [...] Read more.
Traumatic Brain Injury (TBI) mediates neuronal death through several events involving many molecular pathways, including the glutamate-mediated excitotoxicity for excessive stimulation of N-methyl-D-aspartate receptors (NMDARs), producing activation of death signaling pathways. However, the contribution of NMDARs (distribution and signaling-associated to the distribution) remains incompletely understood. We propose a critical role of STEP61 (Striatal-Enriched protein tyrosine phosphatase) in TBI; this phosphatase regulates the dephosphorylated state of the GluN2B subunit through two pathways: by direct dephosphorylation of tyrosine-1472 and indirectly via dephosphorylation and inactivation of Fyn kinase. We previously demonstrated oxidative stress’s contribution to NMDAR signaling and distribution using SOD2+/− mice such a model. We performed TBI protocol using a controlled frontal impact device using C57BL/6 mice and SOD2+/− animals. After TBI, we found alterations in cognitive performance, NMDAR-dependent synaptic function (decreased synaptic form of NMDARs and decreased synaptic current NMDAR-dependent), and increased STEP61 activity. These changes are reduced partially with the STEP61-inhibitor TC-2153 treatment in mice subjected to TBI protocol. This study contributes with evidence about the role of STEP61 in the neuropathological progression after TBI and also the alteration in their activity, such as an early biomarker of synaptic damage in traumatic lesions. Full article
(This article belongs to the Special Issue Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic Brain Injury)
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18 pages, 2859 KiB  
Article
Low Molecular Weight Dextran Sulfate (ILB®) Administration Restores Brain Energy Metabolism Following Severe Traumatic Brain Injury in the Rat
by Giacomo Lazzarino, Angela Maria Amorini, Nicholas M. Barnes, Lars Bruce, Alvaro Mordente, Giuseppe Lazzarino, Valentina Di Pietro, Barbara Tavazzi, Antonio Belli and Ann Logan
Antioxidants 2020, 9(9), 850; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9090850 - 10 Sep 2020
Cited by 10 | Viewed by 3332
Abstract
Traumatic brain injury (TBI) is the leading cause of death and disability in people less than 40 years of age in Western countries. Currently, there are no satisfying pharmacological treatments for TBI patients. In this study, we subjected rats to severe TBI (sTBI), [...] Read more.
Traumatic brain injury (TBI) is the leading cause of death and disability in people less than 40 years of age in Western countries. Currently, there are no satisfying pharmacological treatments for TBI patients. In this study, we subjected rats to severe TBI (sTBI), testing the effects of a single subcutaneous administration, 30 min post-impact, of a new low molecular weight dextran sulfate, named ILB®, at three different dose levels (1, 5, and 15 mg/kg body weight). A group of control sham-operated animals and one of untreated sTBI rats were used for comparison (each group n = 12). On day 2 or 7 post-sTBI animals were sacrificed and the simultaneous HPLC analysis of energy metabolites, N-acetylaspartate (NAA), oxidized and reduced nicotinic coenzymes, water-soluble antioxidants, and biomarkers of oxidative/nitrosative stress was carried out on deproteinized cerebral homogenates. Compared to untreated sTBI rats, ILB® improved energy metabolism by increasing ATP, ATP/ adenosine diphosphate ratio (ATP/ADP ratio), and triphosphate nucleosides, dose-dependently increased NAA concentrations, protected nicotinic coenzyme levels and their oxidized over reduced ratios, prevented depletion of ascorbate and reduced glutathione (GSH), and decreased oxidative (malondialdehyde formation) and nitrosative stress (nitrite + nitrate production). Although needing further experiments, these data provide the first evidence that a single post-injury injection of a new low molecular weight dextran sulfate (ILB®) has beneficial effects on sTBI metabolic damages. Due to the absence of adverse effects in humans, ILB® represents a promising therapeutic agent for the treatment of sTBI patients. Full article
(This article belongs to the Special Issue Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic Brain Injury)
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Review

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34 pages, 10251 KiB  
Review
Antioxidant Therapies in Traumatic Brain Injury
by Valentina Di Pietro, Kamal M. Yakoub, Giuseppe Caruso, Giacomo Lazzarino, Stefano Signoretti, Aron K. Barbey, Barbara Tavazzi, Giuseppe Lazzarino, Antonio Belli and Angela Maria Amorini
Antioxidants 2020, 9(3), 260; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9030260 - 22 Mar 2020
Cited by 67 | Viewed by 6801
Abstract
Due to a multiplicity of causes provoking traumatic brain injury (TBI), TBI is a highly heterogeneous pathology, characterized by high mortality and disability rates. TBI is an acute neurodegenerative event, potentially and unpredictably evolving into sub-chronic and chronic neurodegenerative events, with transient or [...] Read more.
Due to a multiplicity of causes provoking traumatic brain injury (TBI), TBI is a highly heterogeneous pathology, characterized by high mortality and disability rates. TBI is an acute neurodegenerative event, potentially and unpredictably evolving into sub-chronic and chronic neurodegenerative events, with transient or permanent neurologic, cognitive, and motor deficits, for which no valid standardized therapies are available. A vast body of literature demonstrates that TBI-induced oxidative/nitrosative stress is involved in the development of both acute and chronic neurodegenerative disorders. Cellular defenses against this phenomenon are largely dependent on low molecular weight antioxidants, most of which are consumed with diet or as nutraceutical supplements. A large number of studies have evaluated the efficacy of antioxidant administration to decrease TBI-associated damage in various animal TBI models and in a limited number of clinical trials. Points of weakness of preclinical studies are represented by the large variability in the TBI model adopted, in the antioxidant tested, in the timing, dosages, and routes of administration used, and in the variety of molecular and/or neurocognitive parameters evaluated. The analysis of the very few clinical studies does not allow strong conclusions to be drawn on the real effectiveness of antioxidant administration to TBI patients. Standardizing TBI models and different experimental conditions, as well as testing the efficacy of administration of a cocktail of antioxidants rather than only one, should be mandatory. According to some promising clinical results, it appears that sports-related concussion is probably the best type of TBI to test the benefits of antioxidant administration. Full article
(This article belongs to the Special Issue Oxidative and Nitrosative Stress Related to Mitochondrial Dysfunction in Traumatic Brain Injury)
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