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Oxidative Stress and Brain Injury 2.0
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Oxidative Stress and Brain Injury 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 13709

Special Issue Editor

Prof. Dr. Vittorio Fineschi

E-Mail Website
Guest Editor
Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Viale Regina Elena 336, 00161 Rome, RM, Italy
Interests: forensic pathology; sudden cardiac death; molecular mechanisms; traumatic brain injury & oxidative stress; immunohistochemistry; drugs of abuse; oxidative stress; maternal mortality; miRNA; forensic pathologies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue “Oxidative Stress and Brain Injury”.

The scientific literature has given extensive prominence to the effects of reactive oxygen species (ROS) and their induction of oxidative stress and fatal effects on the brain following injury by endogenous factors, traumatic brain injury, and degenerative neural injury due to ROS. Oxidative stress is an event caused by an imbalance between biochemical processes, leading to the production of ROS and those elements responsible for the removal of ROS, known as the enzymatic and non-enzymatic antioxidant cellular defense systems. The excessive production of ROS due to excitotoxicity and depletion of the endogenous antioxidant system induces peroxidation of cellular and vascular structures, protein oxidation, and inhibition of the mitochondrial electron transport chain, causing oxidative cellular damage. Oxidative stress induces cell membrane lipoperoxidation and calcium release, which activates calpain. ROS and RNS induce oxidative damage in neuronal mitochondria and compromise Ca2+ homeostasis. Increase in the defense mechanisms through the use of exogenous antioxidants may be neuroprotective, particularly if they are given within the neuroprotective time window. As an example, a promising potential therapeutic target in DAI is to directly address mitochondria-related injury or to modulate energetic axonal energy failure. However, dietary supplementation with antioxidants and the use of pharmacological agents targeting oxidative stress seem logical, but the benefits of proven antioxidant strategies have not been clearly demonstrated to date.

In this Special Issue on “Oxidative Stress and Brain Injury”, we invite front-line researchers and investigators to submit both original research and review articles regarding the following potential topics, but not limited to:

  • Measurement of ROS;
  • Pathology of brain injuries;
  • Traumatic brain injuries;
  • Hypoxic–ischemic brain damage;
  • Experimental model of brain injuries;
  • Targeted therapy of brain injuries;
  • Drug of abuse and ROS;
  • Histological diagnosis of brain injuries;
  • Epigenetic of brain injuries;
  • miRNA and prognosis of neural damage;
  • Novel approach and proof of principle in therapy;
  • Related quality of life after brain injuries.

Prof. Dr. Vittorio Fineschi
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

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Published Papers (3 papers)

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Research

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14 pages, 1024 KiB  
Article
Biochemical and Behavioral Consequences of Ethanol Intake in a Mouse Model of Metabolic Syndrome
by Pablo Baliño, Ricard Romero-Cano and María Muriach
Int. J. Mol. Sci. 2021, 22(2), 807; https://doi.org/10.3390/ijms22020807 - 15 Jan 2021
Cited by 3 | Viewed by 2171
Abstract
Ethanol abuse is a common issue in individuals with sedentary lifestyles, unbalanced diets, and metabolic syndrome. Both ethanol abuse and metabolic syndrome have negative impacts on the central nervous system, with effects including cognitive impairment and brain oxidative status deterioration. The combined effects [...] Read more.
Ethanol abuse is a common issue in individuals with sedentary lifestyles, unbalanced diets, and metabolic syndrome. Both ethanol abuse and metabolic syndrome have negative impacts on the central nervous system, with effects including cognitive impairment and brain oxidative status deterioration. The combined effects of ethanol abuse and metabolic syndrome at a central level have not yet been elucidated in detail. Thus, this work aims to determine the effects of ethanol intake on a mouse model of metabolic syndrome at the behavioral and biochemical levels. Seven-week-old male control (B6.V-Lep ob/+JRj) and leptin-deficient (metabolic syndrome) (B6.V-Lep ob/obJRj) mice were used in the study. Animals were divided into four groups: control, ethanol, obese, and obese–ethanol. Ethanol consumption was monitored for 6 weeks. Basal glycemia, insulin, and glucose overload tests were performed. To assess short- and long-term memory, an object recognition test was used. In order to assess oxidative status in mouse brain samples, antioxidant enzyme activity was analyzed with regard to glutathione peroxidase, glutathione reductase, glutathione, glutathione disulfide, lipid peroxidation products, and malondialdehyde. Ethanol intake modulated the insulin response and impaired the oxidative status in the ob mouse brain. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 2.0)
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18 pages, 2952 KiB  
Article
Platinum-Based Drugs Cause Mitochondrial Dysfunction in Cultured Dorsal Root Ganglion Neurons
by Markus Leo, Linda-Isabell Schmitt, Patricia Küsterarent, Andrea Kutritz, Tienush Rassaf, Christoph Kleinschnitz, Ulrike B. Hendgen-Cotta and Tim Hagenacker
Int. J. Mol. Sci. 2020, 21(22), 8636; https://doi.org/10.3390/ijms21228636 - 16 Nov 2020
Cited by 25 | Viewed by 3603
Abstract
Cisplatin and oxaliplatin are treatment options for a variety of cancer types. While highly efficient in killing cancer cells, both chemotherapeutics cause severe side effects, e.g., peripheral neuropathies. Using a cell viability assay, a mitochondrial stress assay, and live-cell imaging, the effects of [...] Read more.
Cisplatin and oxaliplatin are treatment options for a variety of cancer types. While highly efficient in killing cancer cells, both chemotherapeutics cause severe side effects, e.g., peripheral neuropathies. Using a cell viability assay, a mitochondrial stress assay, and live-cell imaging, the effects of cis- or oxaliplatin on the mitochondrial function, reactive oxygen species (ROS) production, and mitochondrial and cytosolic calcium concentration of transient receptor potential ankyrin 1 (TRPA1)- or vanilloid 1 (TRPV1)-positive dorsal root ganglion (DRG) neurons of adult Wistar rats were determined. Mitochondrial functions were impaired after exposure to cis- or oxaliplatin by mitochondrial respiratory chain complex I-III inhibition. The basal respiration, spare respiratory capacity, and the adenosine triphosphate (ATP)-linked respiration were decreased after exposure to 10 µM cis- or oxaliplatin. The ROS production showed an immediate increase, and after reaching the peak, ROS production dropped. Calcium imaging showed an increase in the cytosolic calcium concentration during exposure to 10 µM cis- or oxaliplatin in TRPA1- or TRPV1-positive DRG neurons while the mitochondrial calcium concentration continuously decreased. Our data demonstrate a significant effect of cis- and oxaliplatin on mitochondrial function as an early event of platinum-based drug exposure, suggesting mitochondria as a potential target for preventing chemotherapy-induced neuropathy. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 2.0)
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Review

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29 pages, 5194 KiB  
Review
Post-Traumatic Meningitis Is a Diagnostic Challenging Time: A Systematic Review Focusing on Clinical and Pathological Features
by Raffaele La Russa, Aniello Maiese, Nicola Di Fazio, Alessandra Morano, Carlo Di Bonaventura, Alessandra De Matteis, Valentina Fazio, Paola Frati and Vittorio Fineschi
Int. J. Mol. Sci. 2020, 21(11), 4148; https://doi.org/10.3390/ijms21114148 - 10 Jun 2020
Cited by 23 | Viewed by 6973
Abstract
Post-traumatic meningitis is a dreadful condition that presents additional challenges, in terms of both diagnosis and management, when compared with community-acquired cases. Post-traumatic meningitis refers to a meningeal infection causally related to a cranio-cerebral trauma, regardless of temporal proximity. The PICO (participants, intervention, [...] Read more.
Post-traumatic meningitis is a dreadful condition that presents additional challenges, in terms of both diagnosis and management, when compared with community-acquired cases. Post-traumatic meningitis refers to a meningeal infection causally related to a cranio-cerebral trauma, regardless of temporal proximity. The PICO (participants, intervention, control, and outcomes) question was as follows: “Is there an association between traumatic brain injury and post-traumatic meningitis?” The present systematic review was carried out according to the Preferred Reporting Items for Systematic Review (PRISMA) standards. Studies examining post-traumatic meningitis, paying particular attention to victims of traumatic brain injury, were included. Post-traumatic meningitis represents a high mortality disease. Diagnosis may be difficult both because clinical signs are nonspecific and blurred and because of the lack of pathognomonic laboratory markers. Moreover, these markers increase with a rather long latency, thus not allowing a prompt diagnosis, which could improve patients’ outcome. Among all the detectable clinical signs, the appearance of cranial cerebrospinal fluid (CSF) leakage (manifesting as rhinorrhea or otorrhea) should always arouse suspicion of meningitis. On one hand, microbiological exams on cerebrospinal fluid (CSF), which represent the gold standard for the diagnosis, require days to get reliable results. On the other hand, radiological exams, especially CT of the brain, could represent an alternative for early diagnosis. An update on these issues is certainly of interest to focus on possible predictors of survival and useful tools for prompt diagnosis. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 2.0)
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