Antioxidants in Neurons

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

Deadline for manuscript submissions: closed (1 May 2022) | Viewed by 11728

Special Issue Editor

Research Center of Neurology, Volokolamskoe shosse 80, 125367 Moscow, Russia
Interests: cultured neurones; ischemia; traumatic brain injury; ions; neuroprotection

Special Issue Information

Most neurons in the mammalian brain remain functionally active for many decades, possessing complex mechanisms that ensure the preservation of cell viability and functionality. High metabolic and mitochondrial activity of neurons, as well as frequent shifts in the intracellular ion balance, imposes a number of requirements on the brain, including the task of neutralizing the associated reactive oxygen species to prevent oxidative damage. Neurons have a relatively weak internal antioxidant system. Their electrical activity is associated with the regulation of the antioxidant defense system of neurons. In addition, they are able to engage astrocytes in providing antioxidant support to nearby neurons. As a result, both of these ways of maintaining antioxidant defense in neurons and astrocytes contribute to increasing the resistance of neurons to oxidative injury.

This Special issue aims to publish current research related to all aspects of the study of the role of antioxidants in neurons. Researchers are invited to submit original research articles and reviews to this Special Issue.

Dr. Elena V. Stelmashook
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.

Keywords

  • • neurons • antioxidants • astroglia • free radicals

Published Papers (5 papers)

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Research

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17 pages, 3864 KiB  
Article
Glutathione Regulates GPx1 Expression during CA1 Neuronal Death and Clasmatodendrosis in the Rat Hippocampus following Status Epilepticus
by Ji-Eun Kim, Duk-Shin Lee, Tae-Hyun Kim and Tae-Cheon Kang
Antioxidants 2022, 11(4), 756; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11040756 - 11 Apr 2022
Cited by 8 | Viewed by 1881
Abstract
Glutathione peroxidase-1 (GPx1) catalyze the reduction of H2O2 by using glutathione (GSH) as a cofactor. However, the profiles of altered GPx1 expression in response to status epilepticus (SE) have not been fully explored. In the present study, GPx1 expression was [...] Read more.
Glutathione peroxidase-1 (GPx1) catalyze the reduction of H2O2 by using glutathione (GSH) as a cofactor. However, the profiles of altered GPx1 expression in response to status epilepticus (SE) have not been fully explored. In the present study, GPx1 expression was transiently decreased in dentate granule cells, while it was temporarily enhanced and subsequently reduced in CA1 neurons following SE. GPx1 expression was also transiently declined in CA1 astrocytes (within the stratum radiatum) following SE. However, it was elevated in reactive CA1 astrocytes, but not in clasmatodendritic CA1 astrocytes, in chronic epilepsy rats. Under physiological condition, L-buthionine sulfoximine (BSO, an inducer of GSH depletion) increased GPx1 expression in CA1 neurons but decreased it in CA1 astrocytes. However, N-acetylcysteine (NAC, an inducer of GSH synthesis) did not influence GPx1 expression in these cell populations. Following SE, BSO aggravated CA1 neuronal death, concomitant with reduced GPx1 expression. Further. BSO also lowered GPx1 expression in CA1 astrocytes. NAC effectively prevented neuronal death and GPx1 downregulation in CA1 neurons, and restored GPx1 expression to the control level in CA1 astrocytes. In chronic epilepsy rats, BSO reduced GPx1 intensity and exacerbated clasmatodendritic degeneration in CA1 astrocytes. In contrast, NAC restored GPx1 expression in clasmatodendritic astrocytes and ameliorated this autophagic astroglial death. To the best of our knowledge, our findings report, for the first time, the spatiotemporal profiles of altered GPx1 expression in the rat hippocampus following SE, and suggest GSH-mediated GPx1 regulation, which may affect SE-induced neuronal death and autophagic astroglial degeneration. Full article
(This article belongs to the Special Issue Antioxidants in Neurons)
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18 pages, 11264 KiB  
Article
Influence of N-Arachidonoyl Dopamine and N-Docosahexaenoyl Dopamine on the Expression of Neurotrophic Factors in Neuronal Differentiated Cultures of Human Induced Pluripotent Stem Cells under Conditions of Oxidative Stress
by Ekaterina Novosadova, Oleg Dolotov, Ludmila Inozemtseva, Ludmila Novosadova, Stanislav Antonov, Darya Shimchenko, Vladimir Bezuglov, Anna Vetchinova, Vyacheslav Tarantul, Igor Grivennikov and Sergey Illarioshkin
Antioxidants 2022, 11(1), 142; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11010142 - 10 Jan 2022
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Abstract
Oxidative stress (OS) is implicated in the pathogenesis of several neurodegenerative diseases. We have previously shown that N-acyl dopamines (N-ADA and N-DDA) protect the neural cells of healthy donors and patients with Parkinson’s disease from OS. In this study, we assessed the effects [...] Read more.
Oxidative stress (OS) is implicated in the pathogenesis of several neurodegenerative diseases. We have previously shown that N-acyl dopamines (N-ADA and N-DDA) protect the neural cells of healthy donors and patients with Parkinson’s disease from OS. In this study, we assessed the effects of N-acyl dopamines on the expression of neurotrophic factors in human-induced pluripotent stem cell-derived neuronal cultures enriched with dopaminergic neurons under conditions of OS induced by hydrogen peroxide. We showed that hydrogen peroxide treatment increased BDNF but not GDNF mRNA levels, while it did not affect the secretion of corresponding proteins into the culture medium of these cells. Application of N-acyl dopamines promoted BDNF release into the culture medium. Under conditions of OS, N-DDA also increased TRKB, TRKC and RET mRNA levels. Furthermore, N-acyl dopamines prevented cell death 24 h after OS induction and promoted the expression of antioxidant enzymes GPX1, GPX7, SOD1, SOD2 and CAT, as well as reduced the BAX/BCL2 mRNA ratio. These findings indicate that stimulation of the expression of neurotrophic factors and their receptors may underlie the neuroprotective effects of N-acyl dopamines in human neurons. Full article
(This article belongs to the Special Issue Antioxidants in Neurons)
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16 pages, 2725 KiB  
Article
Plant Extract of Limonium gmelinii Attenuates Oxidative Responses in Neurons, Astrocytes, and Cerebral Endothelial Cells In Vitro and Improves Motor Functions of Rats after Middle Cerebral Artery Occlusion
by Tulendy Nurkenov, Andrey Tsoy, Farkhad Olzhayev, Elvira Abzhanova, Anel Turgambayeva, Aizhan Zhussupova, Bharathi Avula, Samir Ross, Aigerim Aituarova, Dariya Kassymova, Galiya Zhusupova, Tamara Shalakhmetova, Tursonjan Tokay, James C. Lee and Sholpan Askarova
Antioxidants 2021, 10(11), 1814; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111814 - 15 Nov 2021
Cited by 4 | Viewed by 2086
Abstract
There are numerous publications demonstrating that plant polyphenols can reduce oxidative stress and inflammatory processes in the brain. In the present study we have investigated the neuroprotective effect of plant extract isolated from the roots of L. gmelinii since it contains a rich [...] Read more.
There are numerous publications demonstrating that plant polyphenols can reduce oxidative stress and inflammatory processes in the brain. In the present study we have investigated the neuroprotective effect of plant extract isolated from the roots of L. gmelinii since it contains a rich source of polyphenols and other biologically active compounds. We have applied an oxidative and inflammatory model induced by NMDA, H2O2, and TNF-α in human primary neurons and astrocytes, and mouse cerebral endothelial cell (CECs) line in vitro. The levels of ROS generation, NADPH oxidase activation, P-selectin expression, and activity of ERK1/2 were evaluated by quantitative immunofluorescence analysis, confocal microscopy, and MAPK assay. In vivo, sensorimotor functions in rats with middle cerebral artery occlusion (MCAO) were assessed. In neurons NMDA induced overproduction of ROS, in astrocytes TNF-α initiated ROS generation, NADPH oxidase activation, and phosphorylation of ERK1/2. In CECs, the exposure by TNF-α induced oxidative stress and triggered the accumulation of P-selectin on the surface of the cells. In turn, pre-treatment of the cells with the extract of L. gmelinii suppressed oxidative stress in all cell types and pro-inflammatory responses in astrocytes and CECs. In vivo, the treatment with L. gmelinii extract improved motor activity in rats with MCAO. Full article
(This article belongs to the Special Issue Antioxidants in Neurons)
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18 pages, 2159 KiB  
Article
Effects of Panthenol and N-Acetylcysteine on Changes in the Redox State of Brain Mitochondria under Oxidative Stress In Vitro
by Dmitry S. Semenovich, Egor Yu. Plotnikov, Oksana V. Titko, Elena P. Lukiyenko and Nina P. Kanunnikova
Antioxidants 2021, 10(11), 1699; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111699 - 27 Oct 2021
Cited by 8 | Viewed by 2294
Abstract
The glutathione system in the mitochondria of the brain plays an important role in maintaining the redox balance and thiol–disulfide homeostasis, whose violations are the important component of the biochemical shifts in neurodegenerative diseases. Mitochondrial dysfunction is known to be accompanied by the [...] Read more.
The glutathione system in the mitochondria of the brain plays an important role in maintaining the redox balance and thiol–disulfide homeostasis, whose violations are the important component of the biochemical shifts in neurodegenerative diseases. Mitochondrial dysfunction is known to be accompanied by the activation of free radical processes, changes in energy metabolism, and is involved in the induction of apoptotic signals. The formation of disulfide bonds is a leading factor in the folding and maintenance of the three-dimensional conformation of many specific proteins that selectively accumulate in brain structures during neurodegenerative pathology. In this study, we estimated brain mitochondria redox status and functioning during induction of oxidative damage in vitro. We have shown that the development of oxidative stress in vitro is accompanied by inhibition of energy metabolism in the brain mitochondria, a shift in the redox potential of the glutathione system to the oxidized side, and activation of S-glutathionylation of proteins. Moreover, we studied the effects of pantothenic acid derivatives—precursors of coenzyme A (CoA), primarily D-panthenol, that exhibit high neuroprotective activity in experimental models of neurodegeneration. Panthenol contributes to the significant restoration of the activity of enzymes of mitochondrial energy metabolism, normalization of the redox potential of the glutathione system, and a decrease in the level of S-glutathionylated proteins in brain mitochondria. The addition of succinate and glutathione precursor N-acetylcysteine enhances the protective effects of the drug. Full article
(This article belongs to the Special Issue Antioxidants in Neurons)
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Review

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23 pages, 1119 KiB  
Review
The Hidden Notes of Redox Balance in Neurodegenerative Diseases
by Silvia Piccirillo, Simona Magi, Alessandra Preziuso, Tiziano Serfilippi, Giorgia Cerqueni, Monia Orciani, Salvatore Amoroso and Vincenzo Lariccia
Antioxidants 2022, 11(8), 1456; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11081456 - 26 Jul 2022
Cited by 5 | Viewed by 2914
Abstract
Reactive oxygen species (ROS) are versatile molecules that, even if produced in the background of many biological processes and responses, possess pleiotropic roles categorized in two interactive yet opposite domains. In particular, ROS can either function as signaling molecules that shape physiological cell [...] Read more.
Reactive oxygen species (ROS) are versatile molecules that, even if produced in the background of many biological processes and responses, possess pleiotropic roles categorized in two interactive yet opposite domains. In particular, ROS can either function as signaling molecules that shape physiological cell functions, or act as deleterious end products of unbalanced redox reactions. Indeed, cellular redox status needs to be tightly regulated to ensure proper cellular functioning, and either excessive ROS accumulation or the dysfunction of antioxidant systems can perturb the redox homeostasis, leading to supraphysiological concentrations of ROS and potentially harmful outcomes. Therefore, whether ROS would act as signaling molecules or as detrimental factors strictly relies on a dynamic equilibrium between free radical production and scavenging resources. Of notice, the mammalian brain is particularly vulnerable to ROS-mediated toxicity, because it possesses relatively poor antioxidant defenses to cope with the redox burden imposed by the elevated oxygen consumption rate and metabolic activity. Many features of neurodegenerative diseases can in fact be traced back to causes of oxidative stress, which may influence both the onset and progression of brain demise. This review focuses on the description of the dual roles of ROS as double-edge sword in both physiological and pathological settings, with reference to Alzheimer’s and Parkinson’s diseases. Full article
(This article belongs to the Special Issue Antioxidants in Neurons)
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