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Antioxidants
Special Issues
Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction
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Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction

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 (1 April 2023) | Viewed by 27645

Special Issue Editors

Prof. Dr. Chongshan Dai

E-Mail Website
Guest Editor
Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China
Interests: antioxidants; oxidative stress; molecular mechanism; autophagy; ferroptosis; neurotoxicity
Special Issues, Collections and Topics in MDPI journals
Dr. Shusheng Tang

E-Mail Website
Guest Editor
Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China
Interests: oxidative stress; molecular mechanism; toxicology; risk assessment; neurotoxicity

Special Issue Information

Dear Colleagues,

Neurotoxicity can be induced by many drugs and environmental toxins, including antibacterial drugs (e.g., colistin, and cefepime), anticancer drugs (e.g., paclitaxel, bortezomib, and cisplatin), heavy metals (e.g., cadmium, copper, and lead), and pathogenic toxins (e.g., lipopolysaccharide [LPS], T-2 toxin, and deoxynivalenol), finally resulting in the development of irreversible neurodegeneration and even death in humans and animals. Understanding the precise molecular mechanisms involved in neurotoxicity is essential to the development of effective agents and novel therapeutic strategies for its treatment. Cellular oxidative stress is a consequence of an imbalance between the generation and detoxification of reactive oxygen species (ROS). The nervous tissue is highly vulnerable to oxidative damage due to its high energy demand, high oxygen consumption, and abundance of peroxidiable fatty acids. In addition, mitochondria, the ‘power plant’ of cells, are the main producer and target of cellular ROS. Oxidative stress usually causes mitochondrial dysfunction and, which is often implicated during neurotoxicity and neurological diseases, but effective mechanism-based therapies remain elusive.

Therefore, this Special Issue aims to collate innovative original research and review articles that reveal new pathogenic pathways, potential therapeutic strategies, and neuroprotective agents, particularly focusing on oxidative stress, mitochondrial dysfunction, and their crosstalk to clarify and ameliorate drugs- or toxin-induced neurotoxicity.

Dr. Chongshan Dai
Dr. Shusheng Tang
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

  • oxidative stress
  • mitochondrial dysfunction
  • neurotoxicity
  • molecular mechanism
  • neuroprotective agents

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Published Papers (6 papers)

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Research

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16 pages, 5447 KiB  
Article
Neuronal Oxidative Stress Promotes α-Synuclein Aggregation In Vivo
by Seok Joon Won, Rebecca Fong, Nicholas Butler, Jennifer Sanchez, Yiguan Zhang, Candance Wong, Olive Tambou Nzoutchoum, Annie Huynh, June Pan and Raymond A. Swanson
Antioxidants 2022, 11(12), 2466; https://doi.org/10.3390/antiox11122466 - 15 Dec 2022
Cited by 14 | Viewed by 2297
Abstract
Both genetic and environmental factors increase risk for Parkinson’s disease. Many of the known genetic factors influence α-synuclein aggregation or degradation, whereas most of the identified environmental factors produce oxidative stress. Studies using in vitro approaches have identified mechanisms by which oxidative stress [...] Read more.
Both genetic and environmental factors increase risk for Parkinson’s disease. Many of the known genetic factors influence α-synuclein aggregation or degradation, whereas most of the identified environmental factors produce oxidative stress. Studies using in vitro approaches have identified mechanisms by which oxidative stress can accelerate the formation of α-synuclein aggregates, but there is a paucity of evidence supporting the importance of these processes over extended time periods in brain. To assess this issue, we evaluated α-synuclein aggregates in brains of three transgenic mouse strains: hSyn mice, which overexpress human α-synuclein in neurons and spontaneously develop α-synuclein aggregates; EAAT3−/− mice, which exhibit a neuron-specific impairment in cysteine uptake and resultant neuron-selective chronic oxidative stress; and double-transgenic hSyn/EAAT3−/− mice. Aggregate formation was evaluated by quantitative immunohistochemistry for phosphoserine 129 α-synuclein and by an α-synuclein proximity ligation assay. Both methods showed that the double transgenic hSyn/EAAT3−/− mice exhibited a significantly higher α-synuclein aggregate density than littermate hSyn mice in each brain region examined. Negligible aggregate formation was observed in the EAAT3−/− mouse strain, suggesting a synergistic rather than additive interaction between the two genotypes. A similar pattern of results was observed in assessments of motor function: the pole test and rotarod test. Together, these observations indicate that chronic, low-grade neuronal oxidative stress promotes α-synuclein aggregate formation in vivo. This process may contribute to the mechanism by which environmentally induced oxidative stress contributes to α-synuclein pathology in idiopathic Parkinson’s disease. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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19 pages, 4236 KiB  
Article
Dim Blue Light at Night Induces Spatial Memory Impairment in Mice by Hippocampal Neuroinflammation and Oxidative Stress
by Qi Liu, Zixu Wang, Jing Cao, Yulan Dong and Yaoxing Chen
Antioxidants 2022, 11(7), 1218; https://doi.org/10.3390/antiox11071218 - 22 Jun 2022
Cited by 19 | Viewed by 3344
Abstract
Light pollution is one of the most serious public problems, especially the night light. However, the effect of dim blue light at night (dLAN-BL) on cognitive function is unclear. In this study, we evaluated the effects of exposure to dLAN-BL in C57BL/6J mice [...] Read more.
Light pollution is one of the most serious public problems, especially the night light. However, the effect of dim blue light at night (dLAN-BL) on cognitive function is unclear. In this study, we evaluated the effects of exposure to dLAN-BL in C57BL/6J mice for 4 consecutive weeks. Our results showed dLAN-BL significantly impaired spatial learning and memory and increased plasma corticosterone level in mice. Consistent with these changes, we observed dLAN-BL significantly increased the numbers and activation of microglia and the levels of oxidative stress product MDA in the hippocampus, decreased the levels of antioxidant enzymes Glutathione peroxidase (GSH-Px), Superoxide dismutase (SOD), Gluathione reductase (Gsr), total antioxidants (T-AOC) and the number of neurons in the hippocampus, up-regulated the mRNA expression levels of IL6, TNF-α and the protein expression levels of iNOS, COX2, TLR4, p-p65, Cleaved-Caspase3 and BAX, and down-regulated the mRNA expression levels of IL4, IL10, Psd95, Snap25, Sirt1, Dcx and the protein expression level of BCL2. In vitro results further showed corticosterone (10uM)-induced BV2 cell activation and up-regulated content of IL6, TNF-α in the cell supernatant and the protein expression levels of iNOS, COX2, p-p65 in BV2 cells. Our findings suggested dLAN-BL up-regulated plasma corticosterone level and hippocampal microglia activation, which in turn caused oxidative stress and neuroinflammation, leading to neuronal loss and synaptic dysfunction, ultimately leading to spatial learning and memory dysfunction in mice. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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Review

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31 pages, 1833 KiB  
Review
Metabolic Priming as a Tool in Redox and Mitochondrial Theragnostics
by Sónia A. Pinho, Sandra I. Anjo and Teresa Cunha-Oliveira
Antioxidants 2023, 12(5), 1072; https://doi.org/10.3390/antiox12051072 - 10 May 2023
Cited by 3 | Viewed by 3160
Abstract
Theragnostics is a promising approach that integrates diagnostics and therapeutics into a single personalized strategy. To conduct effective theragnostic studies, it is essential to create an in vitro environment that accurately reflects the in vivo conditions. In this review, we discuss the importance [...] Read more.
Theragnostics is a promising approach that integrates diagnostics and therapeutics into a single personalized strategy. To conduct effective theragnostic studies, it is essential to create an in vitro environment that accurately reflects the in vivo conditions. In this review, we discuss the importance of redox homeostasis and mitochondrial function in the context of personalized theragnostic approaches. Cells have several ways to respond to metabolic stress, including changes in protein localization, density, and degradation, which can promote cell survival. However, disruption of redox homeostasis can lead to oxidative stress and cellular damage, which are implicated in various diseases. Models of oxidative stress and mitochondrial dysfunction should be developed in metabolically conditioned cells to explore the underlying mechanisms of diseases and develop new therapies. By choosing an appropriate cellular model, adjusting cell culture conditions and validating the cellular model, it is possible to identify the most promising therapeutic options and tailor treatments to individual patients. Overall, we highlight the importance of precise and individualized approaches in theragnostics and the need to develop accurate in vitro models that reflect the in vivo conditions. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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18 pages, 1518 KiB  
Review
Advances of H2S in Regulating Neurodegenerative Diseases by Preserving Mitochondria Function
by Lina Zhou and Qiang Wang
Antioxidants 2023, 12(3), 652; https://doi.org/10.3390/antiox12030652 - 6 Mar 2023
Cited by 20 | Viewed by 2910
Abstract
Neurotoxicity is induced by different toxic substances, including environmental chemicals, drugs, and pathogenic toxins, resulting in oxidative damage and neurodegeneration in mammals. The nervous system is extremely vulnerable to oxidative stress because of its high oxygen demand. Mitochondria are the main source of [...] Read more.
Neurotoxicity is induced by different toxic substances, including environmental chemicals, drugs, and pathogenic toxins, resulting in oxidative damage and neurodegeneration in mammals. The nervous system is extremely vulnerable to oxidative stress because of its high oxygen demand. Mitochondria are the main source of ATP production in the brain neuron, and oxidative stress-caused mitochondrial dysfunction is implicated in neurodegenerative diseases. H2S was initially identified as a toxic gas; however, more recently, it has been recognized as a neuromodulator as well as a neuroprotectant. Specifically, it modulates mitochondrial activity, and H2S oxidation in mitochondria produces various reactive sulfur species, thus modifying proteins through sulfhydration. This review focused on highlighting the neuron modulation role of H2S in regulating neurodegenerative diseases through anti-oxidative, anti-inflammatory, anti-apoptotic and S-sulfhydration, and emphasized the importance of H2S as a therapeutic molecule for neurological diseases. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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23 pages, 1212 KiB  
Review
Neuroprotective Effect of Melatonin on Sleep Disorders Associated with Parkinson’s Disease
by Xinyu Hu, Jingwen Li, Xinyi Wang, Hanshu Liu, Tao Wang, Zhicheng Lin and Nian Xiong
Antioxidants 2023, 12(2), 396; https://doi.org/10.3390/antiox12020396 - 6 Feb 2023
Cited by 18 | Viewed by 7598
Abstract
Parkinson’s disease (PD) is a complex, multisystem disorder with both neurologic and systemic manifestations, which is usually associated with non-motor symptoms, including sleep disorders. Such associated sleep disorders are commonly observed as REM sleep behavior disorder, insomnia, sleep-related breathing disorders, excessive daytime sleepiness, [...] Read more.
Parkinson’s disease (PD) is a complex, multisystem disorder with both neurologic and systemic manifestations, which is usually associated with non-motor symptoms, including sleep disorders. Such associated sleep disorders are commonly observed as REM sleep behavior disorder, insomnia, sleep-related breathing disorders, excessive daytime sleepiness, restless legs syndrome and periodic limb movements. Melatonin has a wide range of regulatory effects, such as synchronizing circadian rhythm, and is expected to be a potential new circadian treatment of sleep disorders in PD patients. In fact, ongoing clinical trials with melatonin in PD highlight melatonin’s therapeutic effects in this disease. Mechanistically, melatonin plays its antioxidant, anti-inflammatory, anti-excitotoxity, anti-synaptic dysfunction and anti-apoptotic activities. In addition, melatonin attenuates the effects of genetic variation in the clock genes of Baml1 and Per1 to restore the circadian rhythm. Together, melatonin exerts various therapeutic effects in PD but their specific mechanisms require further investigations. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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18 pages, 2250 KiB  
Review
Association between Heavy Metal Exposure and Parkinson’s Disease: A Review of the Mechanisms Related to Oxidative Stress
by Sarita Pyatha, Haesoo Kim, Daeun Lee and Kisok Kim
Antioxidants 2022, 11(12), 2467; https://doi.org/10.3390/antiox11122467 - 15 Dec 2022
Cited by 36 | Viewed by 6915
Abstract
Parkinson’s disease (PD) is a gradually progressing neurodegenerative condition that is marked by a loss of motor coordination along with non-motor features. Although the precise cause of PD has not been determined, the disease condition is mostly associated with the exposure to environmental [...] Read more.
Parkinson’s disease (PD) is a gradually progressing neurodegenerative condition that is marked by a loss of motor coordination along with non-motor features. Although the precise cause of PD has not been determined, the disease condition is mostly associated with the exposure to environmental toxins, such as metals, and their abnormal accumulation in the brain. Heavy metals, such as iron (Fe), mercury (Hg), manganese (Mn), copper (Cu), and lead (Pb), have been linked to PD and contribute to its progression. In addition, the interactions among the components of a metal mixture may result in synergistic toxicity. Numerous epidemiological studies have demonstrated a connection between PD and either single or mixed exposure to these heavy metals, which increase the prevalence of PD. Chronic exposure to heavy metals is related to the activation of proinflammatory cytokines resulting in neuronal loss through neuroinflammation. Similarly, metals disrupt redox homeostasis while inducing free radical production and decreasing antioxidant levels in the substantia nigra. Furthermore, these metals alter molecular processes and result in oxidative stress, DNA damage, mitochondrial dysfunction, and apoptosis, which can potentially trigger dopaminergic neurodegenerative disorders. This review focuses on the roles of Hg, Pb, Mn, Cu, and Fe in the development and progression of PD. Moreover, it explores the plausible roles of heavy metals in neurodegenerative mechanisms that facilitate the development of PD. A better understanding of the mechanisms underlying metal toxicities will enable the establishment of novel therapeutic approaches to prevent or cure PD. Full article
(This article belongs to the Special Issue Oxidative Stress-Induced Neurotoxicity and Mitochondrial Dysfunction)
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