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Neuroprotection and Oxidative Distress

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A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (10 December 2021) | Viewed by 20902

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Special Issue Editors

Dr. María García-Fernández

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Guest Editor

1. Department of Human Physiology, Faculty of Medicine, Campus Teatinos, University of Malaga, 29010 Malaga, Spain
2. Institute of Biomedical Research of Malaga (IBIMA), 29010 Malaga, Spain
Interests: oxidative stress; mitochondria; IGF; neuroprotective; ROS; metabolism

Dr. Elisa Martín-Montañez

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Co-Guest Editor

1. Department of Pharmacology, Faculty of Medicine, Campus Teatinos, University of Malaga, 29010 Malaga, Spain
2. Institute of Biomedical Research of Malaga (IBIMA), 29010 Malaga, Spain
Interests: oxidative stress; neuroprotection; memory enhancement; neurological disorders; pulmonary diseases; iron-deficiency; music therapy
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Special Issue Information

Dear Colleagues,

Within Biology and Medicine the concept of oxidative stress was originally formulated in the 1980s by Sies and others as “an unbalance between oxidants and antioxidants”. Recently, with increases in the volume of research related to redox regulation, signalling and sensing, this new complex concept is redefined as “disruption to redox homeostasis”. The destruction of this cellular homeostasis results not only in oxidative damage to different molecules (proteins, lipids, DNA) and cellular structures, but also in a decline in their functions. This redox circuitry is constituted by numerous elements: 1) the oxidant species, specially the derivatives of O₂, NO etc., generated from mitochondria OXOPH, reticular Cyt 450, cytoplasmic NOS, xanthine oxidase/xanthine dehydrogenase etc; 2) the antioxidant systems as a complex network of substances that includes the different enzymatic (SOD, GPX, catalase, etc.) and non-enzymatic molecules (GSH, vitamins, TR, etc.) that participate in the direct and/or indirect detoxication (GRD, G6PDH, TrxR, etc.); 3) those that eliminate the damaged products (GST, etc.); and 4) regulatory factors (NRF1, 2 HIF, etc.). One of the most vulnerable organs to oxidative damage is the brain, which contains a large amount of polyunsaturated fatty acids and consumes a large amount of oxygen for the synthesis of mitochondrial ATP. Furthermore, the brain contains numerous excitotoxic and auto-oxidizable neurotransmitters, redox active metal loading and a weak antioxidant capacity, along with a limited regenerative capacity and poor residue elimination. An adequate oxidant/antioxidant balance is essential in maintaining brain function in normal ageing. The disruption of this redox balance in the brain could represent the origin or the persistence of some neurodegenerative diseases such as Alzheimer’s, Huntington’s, Parkinson’s Disease, ELA, damage after stroke and more. Furthermore, recently, disturbance in redox homeostasis has been found in other neuropsychiatric diseases including depression, anxiety disorders, schizophrenia, and autism spectrum disorders.

In this Special Issue entitled “Neuroprotection and Oxidative Distress” we welcome authors to submit original research studies and reviews, with the aim to enhance our understanding of brain oxidative biology, mechanisms of oxidative distress and their relationship with neuroprotection. We hope that these contributions will inspire the development of possible antioxidant/neuroprotective drugs to treat various redox-related pathologies.

Dr. María García-Fernández
Dr. Elisa Martín-Montañez
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. Brain Sciences 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 2200 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

ROS
mitochondria
antioxidant
neuroprotection
neurodegeneration
brain
neurological disease
oxidative stress

Published Papers (7 papers)

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Research

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17 pages, 1496 KiB

Open AccessArticle

Changes in Affective Behavior and Oxidative Stress after Binge Alcohol in Male and Female Rats

by Ibanelo Cortez, Patricia S. Brocardo and J. Leigh Leasure

Brain Sci. 2021, 11(9), 1250; https://doi.org/10.3390/brainsci11091250 - 21 Sep 2021

Cited by 2 | Viewed by 1949

Abstract

Binge alcohol consumption and alcohol use disorders (AUD) are prevalent, and there is comorbidity with depression and anxiety. Potential underlying mechanisms include neurophysiological, genetic, and metabolic changes resulting from alcohol exposure. Mood and anxiety disorders are more common among women, but whether females are more susceptible to binge-induced oxidative stress and co-occurring anxiety and depression-like behaviors remains unknown. Here, we used a repeated, weekly binge alcohol paradigm in male and female rats to investigate sex differences in despair and anxiety-like behaviors and brain oxidative stress parameters. A single binge alcohol exposure significantly elevated glutathione (GSH) levels in prefrontal cortex (PFC) of both male and female animals. This was accompanied by increased lipid peroxidation in PFC of both sexes. Repeated (once weekly) binge exposure induced changes in anxiety- and depression-like behaviors in both males and females and increased GSH level in the PFC without detectable oxidative damage. Our findings suggest that repeated binge alcohol exposure influences affect regardless of sex and in the absence of membrane damage. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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15 pages, 2968 KiB

Open AccessArticle

Extra Virgin Oil Polyphenols Improve the Protective Effects of Hydroxytyrosol in an In Vitro Model of Hypoxia-Reoxygenation of Rat Brain

by José Pedro De La Cruz Cortés, Inmaculada Pérez de Algaba, Esther Martín-Aurioles, María Monsalud Arrebola, Laura Ortega-Hombrados, María Dolores Rodríguez-Pérez, María África Fernández-Prior, Alejandra Bermúdez-Oria, Cristina Verdugo and José Antonio González-Correa

Brain Sci. 2021, 11(9), 1133; https://doi.org/10.3390/brainsci11091133 - 26 Aug 2021

Cited by 7 | Viewed by 2227

Abstract

Hydroxytyrosol (HT) is the component primarily responsible for the neuroprotective effect of extra virgin olive oil (EVOO). However, it is less effective on its own than the demonstrated neuroprotective effect of EVOO, and for this reason, it can be postulated that there is an interaction between several of the polyphenols of EVOO. The objective of the study was to assess the possible interaction of four EVOO polyphenols (HT, tyrosol, dihydroxyphenylglycol, and oleocanthal) in an experimental model of hypoxia-reoxygenation in rat brain slices. The lactate dehydrogenase (LDH) efflux, lipid peroxidation, and peroxynitrite production were determined as measures of cell death, oxidative stress, and nitrosative stress, respectively. First, the polyphenols were incubated with the brain slices in the same proportions that exist in EVOO, comparing their effects with those of HT. In all cases, the cytoprotective and antioxidant effects of the combination were greater than those of HT alone. Second, we calculated the concentration–effect curves for HT in the absence or presence of each polyphenol. Tyrosol did not significantly modify any of the variables inhibited by HT. Dihydroxyphenylglycol only increased the cytoprotective effect of HT at 10 µM, while it increased its antioxidant effect at 50 and 100 µM and its inhibitory effect on peroxynitrite formation at all the concentrations tested. Oleocanthal increased the cytoprotective and antioxidant effects of HT but did not modify its inhibitory effect on nitrosative stress. The results of this study show that the EVOO polyphenols DHPG and OLC increase the cytoprotective effect of HT in an experimental model of hypoxia-reoxygenation in rat brain slices, mainly due to a possibly synergistic effect on HT’s antioxidant action. These results could explain the greater neuroprotective effect of EVOO than of the polyphenols alone. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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12 pages, 890 KiB

Open AccessArticle

Impact of Glucocorticoid on a Cellular Model of Parkinson’s Disease: Oxidative Stress and Mitochondrial Function

by Silvia Claros, Antonio Gil, Mauro Martinelli, Nadia Valverde, Estrella Lara, Federica Boraldi, Jose Pavia, Elisa Martín-Montañez and María Garcia-Fernandez

Brain Sci. 2021, 11(8), 1106; https://doi.org/10.3390/brainsci11081106 - 22 Aug 2021

Cited by 6 | Viewed by 2531

Abstract

Stress seems to contribute to the neuropathology of Parkinson’s disease (PD), possibly by dysregulation of the hypothalamic–pituitary–adrenal axis. Oxidative distress and mitochondrial dysfunction are key factors involved in the pathophysiology of PD and neuronal glucocorticoid-induced toxicity. Animal PD models have been generated to study the effects of hormonal stress, but no in vitro model has yet been developed. Our aim was to examine the impact of corticosterone (CORT) administration on a dopaminergic neuronal cell model of PD induced by the neurotoxin MPP⁺, as a new combined PD model based on the marker of endocrine response to stress, CORT, and oxidative-mitochondrial damage. We determined the impact of CORT, MPP⁺ and their co-incubation on reactive oxygen species production (O2^−•), oxidative stress cellular markers (advanced-oxidation protein products and total antioxidant status), mitochondrial function (mitochondrial membrane potential and mitochondrial oxygen consumption rate) and neurodegeneration (Fluoro-Jade staining). Accordingly, the administration of MPP⁺ or CORT individually led to cell damage compared to controls (p < 0.05), as determined by several methods, whereas their co-incubation produced strong cell damage (p < 0.05). The combined model described here could be appropriate for investigating neuropathological hallmarks and for evaluating potential new therapeutic tools for PD patients suffering mild to moderate emotional stress. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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13 pages, 1352 KiB

Open AccessArticle

Glutathione as a Molecular Marker of Functional Impairment in Patients with At-Risk Mental State: 7-Tesla ¹H-MRS Study

by Peter Jeon, Roberto Limongi, Sabrina D. Ford, Cassandra Branco, Michael Mackinley, Maya Gupta, Laura Powe, Jean Théberge and Lena Palaniyappan

Brain Sci. 2021, 11(7), 941; https://doi.org/10.3390/brainsci11070941 - 17 Jul 2021

Cited by 8 | Viewed by 2977

Abstract

A substantial number of individuals with clinical high-risk (CHR) mental state do not transition to psychosis. However, regardless of future diagnostic trajectories, many of these individuals develop poor social and occupational functional outcomes. The levels of glutathione, a crucial cortical antioxidant, may track variations in functional outcomes in early psychosis and prodromal states. Thirteen clinical high-risk and 30 healthy control volunteers were recruited for a 7-Tesla magnetic resonance spectroscopy scan with a voxel positioned within the dorsal anterior cingulate cortex (ACC). Clinical assessment scores were collected to determine if any association was observable with glutathione levels. The Bayesian Spearman’s test revealed a positive association between the Social and Occupational Functioning Assessment Scale (SOFAS) and the glutathione concentration in the clinical high-risk group but not in the healthy control group. After accounting for variations in the SOFAS scores, the CHR group had higher GSH levels than the healthy subjects. This study is the first to use 7-Tesla magnetic resonance spectroscopy to test whether ACC glutathione levels relate to social and occupational functioning in a clinically high-risk group and offers preliminary support for glutathione levels as a clinically actionable marker of prognosis in emerging adults presenting with risk features for various severe mental illnesses. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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Review

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15 pages, 624 KiB

Open AccessReview

Role of Vitamin E and the Orexin System in Neuroprotection

by Maria Ester La Torre, Ines Villano, Marcellino Monda, Antonietta Messina, Giuseppe Cibelli, Anna Valenzano, Daniela Pisanelli, Maria Antonietta Panaro, Nicola Tartaglia, Antonio Ambrosi, Marco Carotenuto, Vincenzo Monda, Giovanni Messina and Chiara Porro

Brain Sci. 2021, 11(8), 1098; https://doi.org/10.3390/brainsci11081098 - 20 Aug 2021

Cited by 14 | Viewed by 3483 | Correction

Abstract

Microglia are the first line of defense at the level of the central nervous system (CNS). Phenotypic change in microglia can be regulated by various factors, including the orexin system. Neuroinflammation is an inflammatory process mediated by cytokines, by the lack of interaction between neurotransmitters and their specific receptors, caused by systemic tissue damage or, more often, associated with direct damage to the CNS. Chronic activation of microglia could lead to long-term neurodegenerative diseases. This review aims to explore how tocopherol (vitamin E) and the orexin system may play a role in the prevention and treatment of microglia inflammation and, consequently, in neurodegenerative diseases thanks to its antioxidant properties. The results of animal and in vitro studies provide evidence to support the use of tocopherol for a reduction in microglia inflammation as well as a greater activation of the orexinergic system. Although there is much in vivo and in vitro evidence of vitamin E antioxidant and protective abilities, there are still conflicting results for its use as a treatment for neurodegenerative diseases that speculate that vitamin E, under certain conditions or genetic predispositions, can be pro-oxidant and harmful. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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15 pages, 7425 KiB

Open AccessReview

The Current Role of Dexmedetomidine as Neuroprotective Agent: An Updated Review

by Zaara Liaquat, Xiaoying Xu, Prince Last Mudenda Zilundu, Rao Fu and Lihua Zhou

Brain Sci. 2021, 11(7), 846; https://doi.org/10.3390/brainsci11070846 - 25 Jun 2021

Cited by 29 | Viewed by 5817

Abstract

Dexmedetomidine, selective α2-adrenergic agonist dexmedetomidine, has been widely used clinically for sedation and anesthesia. The role of dexmedetomidine has been an interesting topic of neonatological and anesthetic research since a series of advantages of dexmedetomidine, such as enhancing recovery from surgery, reducing opioid prescription, decreasing sympathetic tone, inhibiting inflammatory reactions, and protecting organs, were reported. Particularly, an increasing number of animal studies have demonstrated that dexmedetomidine ameliorates the neurological outcomes associated with various brain and spinal cord injuries. In addition, a growing number of clinical trials have reported the efficacy of dexmedetomidine for decreasing the rates of postoperative neurological dysfunction, such as delirium and stroke, which strongly highlights the possibility of dexmedetomidine functioning as a neuroprotective agent for future clinical use. Mechanism studies have linked dexmedetomidine’s neuroprotective properties with its modulation of neuroinflammation, apoptosis, oxidative stress, and synaptic plasticity via the α2-adrenergic receptor, dependently or independently. By reviewing recent advances and preclinical and clinical evidence on the neuroprotective effects of dexmedetomidine, we hope to provide a complete understanding of the above mechanism and provide insights into the potential efficacy of this agent in clinical use for patients. Full article

(This article belongs to the Special Issue Neuroprotection and Oxidative Distress)

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