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Antioxidants
Special Issues
Oxidative Stress and the Central Nervous System
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Oxidative Stress and the Central Nervous System

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: 20 September 2024 | Viewed by 9135

Special Issue Editors

Dr. Claudia Colussi

E-Mail Website
Guest Editor
Istituto di Analisi dei Sistemi ed Informatica, National Research Council (CNR), Rome, Italy
Interests: Alzheimer’s disease; neurogenesis; epigenetics; HDACs; synaptic plasticity
Dr. Marcello D’Ascenzo

E-Mail Website
Guest Editor
Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy
Interests: brain plasticity; neuronal excitability; neuropsychiatric diseases; neurodegenerative diseases; neurophysiological

Special Issue Information

Dear Colleagues,

It is now recognized that changes in the redox balance and an increase in oxidative stress occur during aging and in neurodegenerative illnesses, and that these are common traits that lead to central nervous system cell failure. Reactive oxygen and nitrosative species affect the function of several macromolecules including DNA, lipids and proteins. Specifically, protein post-translational modifications induced either directly by nitroxidative species (e.g., nitration, nitrosylation) or activated by secondary pathways (e.g., ubiquitination, phosphorylation, SUMOylation) have an enormous impact on proteostasis and the proteasome function, leading to protein aggregation, misfolding and inactivation. All of these alterations result in cellular dysfunction, synaptic connection loss and brain injury.

In this Special Issue, we will pay special attention to the impact of oxidative-stress-dependent protein post-translational modifications on protein stability and function and the implications for central nervous system components (neurons, astrocytes, glial cells, stem cells) in aging and neurodegeneration. Both original articles and reviews are welcomed based on in vitro and in vivo studies, focusing on understanding how oxidative stress, through protein alteration (misfolding, aggregation, post-translational modifications, inflammation), impacts the viability and function of the cells of the CNS.

Dr. Claudia Colussi
Dr. Marcello D’Ascenzo
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

  • neurodegeneration
  • aging
  • proteostasis
  • post-translational modifications
  • oxidative stress
  • proteasome

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Published Papers (6 papers)

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20 pages, 7797 KiB  
Article
Administration of Bicarbonate Protects Mitochondria, Rescues Retinal Ganglion Cells, and Ameliorates Visual Dysfunction Caused by Oxidative Stress
by Tonking Bastola, Guy A. Perkins, Viet Anh Nguyen Huu, Saeyeon Ju, Keun-Young Kim, Ziyao Shen, Dorota Skowronska-Krawczyk, Robert N. Weinreb and Won-Kyu Ju
Antioxidants 2024, 13(6), 743; https://doi.org/10.3390/antiox13060743 - 19 Jun 2024
Viewed by 1152
Abstract
Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial protection, promoting RGC survival. Soluble adenylyl cyclase (sAC) is a key [...] Read more.
Oxidative stress is a key factor causing mitochondrial dysfunction and retinal ganglion cell (RGC) death in glaucomatous neurodegeneration. The cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway is involved in mitochondrial protection, promoting RGC survival. Soluble adenylyl cyclase (sAC) is a key regulator of the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway, which is known to protect mitochondria and promote RGC survival. However, the precise molecular mechanisms connecting the sAC-mediated signaling pathway with mitochondrial protection in RGCs against oxidative stress are not well characterized. Here, we demonstrate that sAC plays a critical role in protecting RGC mitochondria from oxidative stress. Using mouse models of oxidative stress induced by ischemic injury and paraquat administration, we found that administration of bicarbonate, as an activator of sAC, protected RGCs, blocked AMP-activated protein kinase activation, inhibited glial activation, and improved visual function. Moreover, we found that this is the result of preserving mitochondrial dynamics (fusion and fission), promoting mitochondrial bioenergetics and biogenesis, and preventing metabolic stress and apoptotic cell death. Notably, the administration of bicarbonate ameliorated mitochondrial dysfunction in RGCs by enhancing mitochondrial biogenesis, preserving mitochondrial structure, and increasing ATP production in oxidatively stressed RGCs. These findings suggest that activating sAC enhances the mitochondrial structure and function in RGCs to counter oxidative stress, consequently promoting RGC protection. We propose that modulation of the sAC-mediated signaling pathway has therapeutic potential acting on RGC mitochondria for treating glaucoma and other retinal diseases. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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21 pages, 635 KiB  
Review
Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment
by Chiara Lubrano, Francesca Parisi and Irene Cetin
Antioxidants 2024, 13(4), 453; https://doi.org/10.3390/antiox13040453 - 11 Apr 2024
Viewed by 1930
Abstract
During intrauterine life, external stimuli including maternal nutrition, lifestyle, socioeconomic conditions, anxiety, stress, and air pollution can significantly impact fetal development. The human brain structures begin to form in the early weeks of gestation and continue to grow and mature throughout pregnancy. This [...] Read more.
During intrauterine life, external stimuli including maternal nutrition, lifestyle, socioeconomic conditions, anxiety, stress, and air pollution can significantly impact fetal development. The human brain structures begin to form in the early weeks of gestation and continue to grow and mature throughout pregnancy. This review aims to assess, based on the latest research, the impact of environmental factors on fetal and neonatal brain development, showing that oxidative stress and inflammation are implied as a common factor for most of the stressors. Environmental insults can induce a maternal inflammatory state and modify nutrient supply to the fetus, possibly through epigenetic mechanisms, leading to significant consequences for brain morphogenesis and neurological outcomes. These risk factors are often synergic and mutually reinforcing. Fetal growth restriction and preterm birth represent paradigms of intrauterine reduced nutrient supply and inflammation, respectively. These mechanisms can lead to an increase in free radicals and, consequently, oxidative stress, with well-known adverse effects on the offspring’s neurodevelopment. Therefore, a healthy intrauterine environment is a critical factor in supporting normal fetal brain development. Hence, healthcare professionals and clinicians should implement effective interventions to prevent and reduce modifiable risk factors associated with an increased inflammatory state and decreased nutrient supply during pregnancy. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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29 pages, 2729 KiB  
Review
Potential of Natural Phenolic Compounds against Doxorubicin-Induced Chemobrain: Biological and Molecular Mechanisms Involved
by Simona Serini and Gabriella Calviello
Antioxidants 2024, 13(4), 486; https://doi.org/10.3390/antiox13040486 - 18 Apr 2024
Viewed by 1291
Abstract
Chemotherapy-induced cognitive impairment or “chemobrain” is a prevalent long-term complication of chemotherapy and one of the more devastating. Most of the studies performed so far to identify the cognitive dysfunctions induced by antineoplastic chemotherapies have been focused on treatment with anthracyclines, frequently administered [...] Read more.
Chemotherapy-induced cognitive impairment or “chemobrain” is a prevalent long-term complication of chemotherapy and one of the more devastating. Most of the studies performed so far to identify the cognitive dysfunctions induced by antineoplastic chemotherapies have been focused on treatment with anthracyclines, frequently administered to breast cancer patients, a population that, after treatment, shows a high possibility of long survival and, consequently, of chemobrain development. In the last few years, different possible strategies have been explored to prevent or reduce chemobrain induced by the anthracycline doxorubicin (DOX), known to promote oxidative stress and inflammation, which have been strongly implicated in the development of this brain dysfunction. Here, we have critically analyzed the results of the preclinical studies from the last few years that have evaluated the potential of phenolic compounds (PheCs), a large class of natural products able to exert powerful antioxidant and anti-inflammatory activities, in inhibiting DOX-induced chemobrain. Several PheCs belonging to different classes have been shown to be able to revert DOX-induced brain morphological damages and deficits associated with learning, memory, and exploratory behavior. We have analyzed the biological and molecular mechanisms implicated and suggested possible future perspectives in this research area. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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23 pages, 9064 KiB  
Article
NHE1 Protein in Repetitive Mild TBI-Mediated Neuroinflammation and Neurological Function Impairment
by John P. Bielanin, Shamseldin A. H. Metwally, Helena C. M. Oft, Satya S. Paruchuri, Lin Lin, Okan Capuk, Nicholas D. Pennock, Shanshan Song and Dandan Sun
Antioxidants 2024, 13(7), 836; https://doi.org/10.3390/antiox13070836 - 13 Jul 2024
Viewed by 642
Abstract
Mild traumatic brain injuries (mTBIs) are highly prevalent and can lead to chronic behavioral and cognitive deficits often associated with the development of neurodegenerative diseases. Oxidative stress and formation of reactive oxygen species (ROS) have been implicated in mTBI-mediated axonal injury and pathogenesis. [...] Read more.
Mild traumatic brain injuries (mTBIs) are highly prevalent and can lead to chronic behavioral and cognitive deficits often associated with the development of neurodegenerative diseases. Oxidative stress and formation of reactive oxygen species (ROS) have been implicated in mTBI-mediated axonal injury and pathogenesis. However, the underlying mechanisms and contributing factors are not completely understood. In this study, we explore these pathogenic mechanisms utilizing a murine model of repetitive mTBI (r-mTBI) involving five closed-skull concussions in young adult C57BL/6J mice. We observed a significant elevation of Na+/H+ exchanger protein (NHE1) expression in GFAP+ reactive astrocytes, IBA1+ microglia, and OLIG2+ oligodendrocytes across various brain regions (including the cerebral cortex, corpus callosum, and hippocampus) after r-mTBI. This elevation was accompanied by astrogliosis, microgliosis, and the accumulation of amyloid precursor protein (APP). Mice subjected to r-mTBI displayed impaired motor learning and spatial memory. However, post-r-mTBI administration of a potent NHE1 inhibitor, HOE642, attenuated locomotor and cognitive functional deficits as well as pathological signatures of gliosis, oxidative stress, axonal damage, and white matter damage. These findings indicate NHE1 upregulation plays a role in r-mTBI-induced oxidative stress, axonal damage, and gliosis, suggesting NHE1 may be a promising therapeutic target to alleviate mTBI-induced injuries and restore neurological function. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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11 pages, 3765 KiB  
Article
Expression of ChAT, Iba-1, and nNOS in the Central Nervous System following Facial Nerve Injury
by Jae Min Lee, Myung Chul Yoo, Yong Jun Kim, Sung Soo Kim and Seung Geun Yeo
Antioxidants 2024, 13(5), 595; https://doi.org/10.3390/antiox13050595 - 12 May 2024
Viewed by 1202
Abstract
Facial nerve injury can cause significant functional impairment, impacting both the peripheral and central nervous systems. The present study evaluated changes in facial motor function, numbers of cholinergic neurons and microglia, and nNOS levels in the facial nucleus of the central nervous system [...] Read more.
Facial nerve injury can cause significant functional impairment, impacting both the peripheral and central nervous systems. The present study evaluated changes in facial motor function, numbers of cholinergic neurons and microglia, and nNOS levels in the facial nucleus of the central nervous system (CNS) following peripheral facial nerve injury. Facial nerve function, as determined by eyeblink and whisker-movement reflexes, was evaluated at baseline and 1, 2, 3, 4, 8, and 12 weeks after inducing facial nerve injury through compression or axotomy. The expression of choline acetyltransferase (ChAT), ionized calcium-binding adaptor molecule 1 (Iba-1), and neuronal nitric oxide synthase (nNOS) in the facial nucleus of the CNS was analyzed 2, 4, and 12 weeks after peripheral facial nerve injury. Compression-induced facial nerve injury was found to lead to temporary facial motor impairment, whereas axotomy resulted in persistent impairment. Moreover, both compression and axotomy reduced ChAT expression and increased Iba-1 and nNOS expression in the facial nucleus, indicating upregulation of an inflammatory response and neurodegeneration. These results indicate that, compared with compression-induced injury, axotomy-induced facial nerve injury results in greater facial motor dysfunction and more persistent microglial and nitric oxide activation in the facial nucleus of the CNS. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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21 pages, 4911 KiB  
Article
Evaluating the Neuroprotective Potential of Caffeinated Coffee in the Context of Aluminum-Induced Neurotoxicity: Insights from a PC12 Cell Culture Model
by Kamil Rodak, Dorota Bęben, Monika Birska, Oliwia Siwiela, Izabela Kokot, Helena Moreira, Anna Radajewska, Anna Szyjka and Ewa Maria Kratz
Antioxidants 2024, 13(3), 342; https://doi.org/10.3390/antiox13030342 - 13 Mar 2024
Cited by 3 | Viewed by 2009
Abstract
Exposure to aluminum (Al) and its compounds is an environmental factor that induces neurotoxicity, partially through oxidative stress, potentially leading to the development of neurodegenerative diseases. Components of the diet, such as caffeinated coffee, may play a significant role in preventing these diseases. [...] Read more.
Exposure to aluminum (Al) and its compounds is an environmental factor that induces neurotoxicity, partially through oxidative stress, potentially leading to the development of neurodegenerative diseases. Components of the diet, such as caffeinated coffee, may play a significant role in preventing these diseases. In the present study, an experimental model of PC12 cells (rat pheochromocytoma tumor cells) was developed to investigate the influence of caffeine and caffeinated coffee on neurotoxicity induced by Al compounds and/or oxidative stress. For the induction of neurotoxicity, aluminum maltolate (Almal) and H2O2 were used. The present study demonstrates that 100 μM Almal reduced cell survival, while caffeinated coffee with caffeine concentrations of 5 μg/mL and 80 μg/mL reversed this effect, resulting in a higher than fivefold increase in PC12 cell survival. However, despite the observed antioxidant properties typical for caffeine and caffeinated coffee, it is unlikely that they are the key factors contributing to cell protection against neurotoxicity induced by both oxidative stress and Al exposure. Moreover, the present study reveals that for coffee to exert its effects, it is possible that Al must first activate certain mechanisms within the cell. Therefore, various signaling pathways are discussed, and modifications of these pathways might significantly decrease the risk of Al-induced neurotoxicity. Full article
(This article belongs to the Special Issue Oxidative Stress and the Central Nervous System)
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