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Neuroprotective Effect of Glutathione 2.0
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Neuroprotective Effect of Glutathione 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 10221

Special Issue Editor

Prof. Dr. Koji Aoyama

E-Mail Website
Guest Editor
Department of Pharmacology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi, Tokyo 173-8605, Japan
Interests: glutathione; RNA; circadian rhythm
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

More than 130 years have passed since glutathione (GSH) was discovered as "philothione" from yeast. There are many publications regarding the neuroprotective functions of GSH (as an antioxidant and/or redox buffer, etc.) in vivo and in vitro, while GSH depletion induces/exacerbates neuronal damage in the brain. The promotion of GSH functions would be a promising approach against neuronal death. The aim of this Special Issue is to provide feature articles of the most current findings related to GSH in the central nervous system. In this Special Issue, neurologic disorders based on molecular sciences related to GSH dysfunction are also encouraged.

Prof. Dr. Koji Aoyama
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.

Published Papers (4 papers)

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Review

21 pages, 1721 KiB  
Review
Glutathione-Mediated Neuroprotective Effect of Purine Derivatives
by Nobuko Matsumura and Koji Aoyama
Int. J. Mol. Sci. 2023, 24(17), 13067; https://doi.org/10.3390/ijms241713067 - 22 Aug 2023
Viewed by 1609
Abstract
Numerous basic studies have reported on the neuroprotective properties of several purine derivatives such as caffeine and uric acid (UA). Epidemiological studies have also shown the inverse association of appropriate caffeine intake or serum urate levels with neurodegenerative diseases such as Alzheimer disease [...] Read more.
Numerous basic studies have reported on the neuroprotective properties of several purine derivatives such as caffeine and uric acid (UA). Epidemiological studies have also shown the inverse association of appropriate caffeine intake or serum urate levels with neurodegenerative diseases such as Alzheimer disease (AD) and Parkinson’s disease (PD). The well-established neuroprotective mechanisms of caffeine and UA involve adenosine A2A receptor antagonism and antioxidant activity, respectively. Our recent study found that another purine derivative, paraxanthine, has neuroprotective effects similar to those of caffeine and UA. These purine derivatives can promote neuronal cysteine uptake through excitatory amino acid carrier protein 1 (EAAC1) to increase neuronal glutathione (GSH) levels in the brain. This review summarizes the GSH-mediated neuroprotective effects of purine derivatives. Considering the fact that GSH depletion is a manifestation in the brains of AD and PD patients, administration of purine derivatives may be a new therapeutic approach to prevent or delay the onset of these neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neuroprotective Effect of Glutathione 2.0)
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28 pages, 8038 KiB  
Review
Critical Roles of the Cysteine–Glutathione Axis in the Production of γ-Glutamyl Peptides in the Nervous System
by Junichi Fujii, Tsukasa Osaki, Yuya Soma and Yumi Matsuda
Int. J. Mol. Sci. 2023, 24(9), 8044; https://doi.org/10.3390/ijms24098044 - 28 Apr 2023
Cited by 5 | Viewed by 2070
Abstract
γ-Glutamyl moiety that is attached to the cysteine (Cys) residue in glutathione (GSH) protects it from peptidase-mediated degradation. The sulfhydryl group of the Cys residue represents most of the functions of GSH, which include electron donation to peroxidases, protection of reactive sulfhydryl in [...] Read more.
γ-Glutamyl moiety that is attached to the cysteine (Cys) residue in glutathione (GSH) protects it from peptidase-mediated degradation. The sulfhydryl group of the Cys residue represents most of the functions of GSH, which include electron donation to peroxidases, protection of reactive sulfhydryl in proteins via glutaredoxin, and glutathione conjugation of xenobiotics, whereas Cys-derived sulfur is also a pivotal component of some redox-responsive molecules. The amount of Cys that is available tends to restrict the capacity of GSH synthesis. In in vitro systems, cystine is the major form in the extracellular milieu, and a specific cystine transporter, xCT, is essential for survival in most lines of cells and in many primary cultivated cells as well. A reduction in the supply of Cys causes GPX4 to be inhibited due to insufficient GSH synthesis, which leads to iron-dependent necrotic cell death, ferroptosis. Cells generally cannot take up GSH without the removal of γ-glutamyl moiety by γ-glutamyl transferase (GGT) on the cell surface. Meanwhile, the Cys–GSH axis is essentially common to certain types of cells; primarily, neuronal cells that contain a unique metabolic system for intercellular communication concerning γ-glutamyl peptides. After a general description of metabolic processes concerning the Cys–GSH axis, we provide an overview and discuss the significance of GSH-related compounds in the nervous system. Full article
(This article belongs to the Special Issue Neuroprotective Effect of Glutathione 2.0)
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13 pages, 3732 KiB  
Review
The Protective Role of Glutathione on Zinc-Induced Neuron Death after Brain Injuries
by Min Kyu Park, Bo Young Choi, A Ra Kho, Song Hee Lee, Dae Ki Hong, Beom Seok Kang, Si Hyun Lee and Sang Won Suh
Int. J. Mol. Sci. 2023, 24(3), 2950; https://doi.org/10.3390/ijms24032950 - 2 Feb 2023
Cited by 7 | Viewed by 2438
Abstract
Glutathione (GSH) is necessary for maintaining physiological antioxidant function, which is responsible for maintaining free radicals derived from reactive oxygen species at low levels and is associated with improved cognitive performance after brain injury. GSH is produced by the linkage of tripeptides that [...] Read more.
Glutathione (GSH) is necessary for maintaining physiological antioxidant function, which is responsible for maintaining free radicals derived from reactive oxygen species at low levels and is associated with improved cognitive performance after brain injury. GSH is produced by the linkage of tripeptides that consist of glutamic acid, cysteine, and glycine. The adequate supplementation of GSH has neuroprotective effects in several brain injuries such as cerebral ischemia, hypoglycemia, and traumatic brain injury. Brain injuries produce an excess of reactive oxygen species through complex biochemical cascades, which exacerbates primary neuronal damage. GSH concentrations are known to be closely correlated with the activities of certain genes such as excitatory amino acid carrier 1 (EAAC1), glutamate transporter-associated protein 3–18 (Gtrap3-18), and zinc transporter 3 (ZnT3). Following brain-injury-induced oxidative stress, EAAC1 function is negatively impacted, which then reduces cysteine absorption and impairs neuronal GSH synthesis. In these circumstances, vesicular zinc is also released into the synaptic cleft and then translocated into postsynaptic neurons. The excessive influx of zinc inhibits glutathione reductase, which inhibits GSH’s antioxidant functions in neurons, resulting in neuronal damage and ultimately in the impairment of cognitive function. Therefore, in this review, we explore the overall relationship between zinc and GSH in terms of oxidative stress and neuronal cell death. Furthermore, we seek to understand how the modulation of zinc can rescue brain-insult-induced neuronal death after ischemia, hypoglycemia, and traumatic brain injury. Full article
(This article belongs to the Special Issue Neuroprotective Effect of Glutathione 2.0)
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Graphical abstract

20 pages, 2019 KiB  
Review
Glutathione Depletion and MicroRNA Dysregulation in Multiple System Atrophy: A Review
by Chisato Kinoshita, Noriko Kubota and Koji Aoyama
Int. J. Mol. Sci. 2022, 23(23), 15076; https://doi.org/10.3390/ijms232315076 - 1 Dec 2022
Cited by 4 | Viewed by 3633
Abstract
Multiple system atrophy (MSA) is a rare neurodegenerative disease characterized by parkinsonism, cerebellar impairment, and autonomic failure. Although the causes of MSA onset and progression remain uncertain, its pathogenesis may involve oxidative stress via the generation of excess reactive oxygen species and/or destruction [...] Read more.
Multiple system atrophy (MSA) is a rare neurodegenerative disease characterized by parkinsonism, cerebellar impairment, and autonomic failure. Although the causes of MSA onset and progression remain uncertain, its pathogenesis may involve oxidative stress via the generation of excess reactive oxygen species and/or destruction of the antioxidant system. One of the most powerful antioxidants is glutathione, which plays essential roles as an antioxidant enzyme cofactor, cysteine-storage molecule, major redox buffer, and neuromodulator, in addition to being a key antioxidant in the central nervous system. Glutathione levels are known to be reduced in neurodegenerative diseases. In addition, genes regulating redox states have been shown to be post-transcriptionally modified by microRNA (miRNA), one of the most important types of non-coding RNA. miRNAs have been reported to be dysregulated in several diseases, including MSA. In this review, we focused on the relation between glutathione deficiency, miRNA dysregulation and oxidative stress and their close relation with MSA pathology. Full article
(This article belongs to the Special Issue Neuroprotective Effect of Glutathione 2.0)
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