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Antioxidants
Special Issues
Oxidative Stress in Brain Function—2nd Edition
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Oxidative Stress in Brain Function—2nd Edition

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: 21 July 2025 | Viewed by 3100

Special Issue Editor

Dr. Waldo Cerpa

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Guest Editor
Laboratorio de Función y Patología Neuronal, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile
Interests: neurobiology; glutamate receptors; traumatic brain injury; alcohol intake
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The different cellular mechanisms that govern complex brain functions are regulated through intrinsic (genetic) or external (environmental) factors. One of the most critical regulatory axes at the cellular level is established around the cellular capacities that counteract the oxidative stress emerging in different pathophysiological contexts. Cellular components, which include cytoplasmic and mitochondrial enzymes (e.g., catalase and MnSOD, respectively), together with specific molecules (e.g., glutathione), fulfill their role in the control of oxidative stress. At the brain level, this control is essential due to the limited capacity of neurons to form new cells. Therefore, brain cells cope very efficiently with oxidative stress, and their functions are only altered when these cellular strategies are overwhelmed.

In the second edition of this Special Issue, we will collate manuscripts that contribute to a better understanding of the cellular mechanisms that prevent oxidative stress and allow for the proper maintenance of brain functions. We invite researchers to submit original research and review articles related to brain function and oxidative stress caused by intrinsic or external factors. Studies in laboratory models and humans will be considered.

We believe that bringing together different methods of studying brain function in the context of oxidative stress is particularly relevant to understanding cellular events. This understanding will contribute not only to the much-needed knowledge in the area, but also the search for diagnostic and therapeutic strategies for diseases in which oxidative stress plays an essential role in controlling brain function.

Dr. Waldo Cerpa
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

  • pathophysiological brain regulation
  • brain function
  • oxidative stress
  • brain damage
  • neurodegeneration
  • cellular signaling
  • neurotoxicity
  • excitotoxicity
  • synaptic transmission
  • cognitive function

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Published Papers (4 papers)

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Research

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19 pages, 3725 KiB  
Article
Neuronal p38 MAPK Signaling Contributes to Cisplatin-Induced Peripheral Neuropathy
by Yugal Goel, Donovan A. Argueta, Kristen Peterson, Naomi Lomeli, Daniela A. Bota and Kalpna Gupta
Antioxidants 2025, 14(4), 445; https://doi.org/10.3390/antiox14040445 - 8 Apr 2025
Viewed by 398
Abstract
This study investigates the role of p38 mitogen-activated protein kinase (MAPK) activation in dorsal root ganglion (DRG) neurons in the development and progression of chemotherapy-induced peripheral neuropathy (CIPN). This research evaluates whether inhibiting activation of p38 MAPK could reduce neuropathic outcomes in a [...] Read more.
This study investigates the role of p38 mitogen-activated protein kinase (MAPK) activation in dorsal root ganglion (DRG) neurons in the development and progression of chemotherapy-induced peripheral neuropathy (CIPN). This research evaluates whether inhibiting activation of p38 MAPK could reduce neuropathic outcomes in a transgenic breast cancer mouse model (C3TAg) and wild-type mice (FVB/N) treated with cisplatin. Cisplatin treatment stimulated p38 MAPK phosphorylation and nuclear translocation in DRG neurons. Neflamapimod, a specific inhibitor of p38 MAPK alpha (p38α), proven to be safe in clinical trials, inhibited neuronal cisplatin-induced p38 MAPK phosphorylation in vitro and in vivo. Neflamapimod also reduced cisplatin-induced oxidative stress, mitochondrial dysfunction, and cleaved caspase-3 expression in DRG neurons in vitro, protecting neuronal integrity and preventing axonal damage. Functionally, neflamapimod improved mechanical and musculoskeletal hyperalgesia, and cold sensitivity in cisplatin-treated mice, reversing neuropathic pain and neurotoxicity. This study identifies p38 MAPK activation as a critical driver of CIPN and highlights its potential as a therapeutic target for CIPN. Targeting p38 MAPK activation with neflamapimod offers a promising strategy to mitigate neurotoxicity and hyperalgesia without exacerbating cancer progression, positioning it as a novel intervention for CIPN. Full article
(This article belongs to the Special Issue Oxidative Stress in Brain Function—2nd Edition)
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28 pages, 4983 KiB  
Article
Agomelatine Alleviates Depressive-like Behaviors by Suppressing Hippocampal Oxidative Stress in the Chronic Social Defeat Stress Model
by Yan Zhu, Ye Li, Zhaoying Yu, Xiao Chen, Tian Lan, Meijian Wang and Shuyan Yu
Antioxidants 2025, 14(4), 410; https://doi.org/10.3390/antiox14040410 - 28 Mar 2025
Viewed by 353
Abstract
Major depressive disorder (MDD) is a common psychiatric disorder characterized by significant mood disturbances and cognitive impairments. Chronic stress, particularly social defeat stress, plays a crucial role in the etiology of depression, with oxidative stress being a pivotal factor in its pathophysiology. Consequently, [...] Read more.
Major depressive disorder (MDD) is a common psychiatric disorder characterized by significant mood disturbances and cognitive impairments. Chronic stress, particularly social defeat stress, plays a crucial role in the etiology of depression, with oxidative stress being a pivotal factor in its pathophysiology. Consequently, identifying effective strategies to mitigate oxidative stress and prevent the progression of depression is of paramount importance. Agomelatine, an atypical antidepressant with melatonergic and serotonergic properties, has shown promise in treating MDD due to its unique mechanisms of action. In this study, we aimed to investigate whether agomelatine could ameliorate behavioral deficits in a chronic social defeat stress (CSDS) mouse model. CSDS mice were administered agomelatine (50 mg/kg, intraperitoneally) and exhibited significant reductions in both anxiety-like and depressive-like behaviors in behavioral tests. Further analysis revealed that agomelatine treatment effectively reduced oxidative damage in the hippocampus of CSDS mice. Additionally, agomelatine attenuated mitochondrial dysfunction and restored synaptic plasticity, as evidenced by an increased density of excitatory synapses and enhanced neuronal activity. These findings suggest that agomelatine may exert therapeutic effects by reducing oxidative stress, preserving mitochondrial function, and enhancing synaptic plasticity, providing new insights into its potential as a treatment for chronic social defeat stress-induced depression. Full article
(This article belongs to the Special Issue Oxidative Stress in Brain Function—2nd Edition)
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22 pages, 4072 KiB  
Article
Oral Administration of Lactobacillus gasseri and Lacticaseibacillus rhamnosus Ameliorates Amyloid Beta (Aβ)-Induced Cognitive Impairment by Improving Synaptic Function Through Regulation of TLR4/Akt Pathway
by Hye Ji Choi, Hyo Lim Lee, In Young Kim, Yeong Hyeon Ju, Yu Mi Heo, Hwa Rang Na, Ji Yeon Lee, Soo-Im Choi and Ho Jin Heo
Antioxidants 2025, 14(2), 139; https://doi.org/10.3390/antiox14020139 - 24 Jan 2025
Cited by 1 | Viewed by 921
Abstract
This study investigated the anti-amnesic effects of Lactobacillus gasseri (L. gasseri) MG4247 and Lacticaseibacillus rhamnosus (L. rhamnosus) MG4644 in amyloid beta (Aβ)-induced mice. We confirmed that oral administration of L. gasseri MG4247 and L. rhamnosus MG4644 ameliorated cognitive impairment [...] Read more.
This study investigated the anti-amnesic effects of Lactobacillus gasseri (L. gasseri) MG4247 and Lacticaseibacillus rhamnosus (L. rhamnosus) MG4644 in amyloid beta (Aβ)-induced mice. We confirmed that oral administration of L. gasseri MG4247 and L. rhamnosus MG4644 ameliorated cognitive impairment in Aβ-induced mice using Y-maze, passive avoidance, and Morris water maze tests. Oral administration of L. gasseri MG4247 and L. rhamnosus MG4644 protected the antioxidant system by regulating superoxide dismutase levels, reduced glutathione levels, and reduced malondialdehyde contents. Similarly, they attenuated mitochondrial function by decreasing mitochondrial reactive oxygen species levels and increasing mitochondrial membrane potential and ATP levels. In addition, they regulated neuroinflammation and neurotoxicity by modulating the Toll-like receptor 4 (TLR4)/protein kinase B (Akt) pathway. As a result, they enhanced synaptic function by regulating acetylcholine contents, acetylcholinesterase activity, and the expression of synaptic-function-related proteins such as AChE, ChAT, SYP, PSD-95, and GAP-43. Furthermore, the administration of L. gasseri MG4247 and L. rhamnosus MG4644 improved dysbiosis by promoting the growth of beneficial bacteria while suppressing the growth of harmful bacteria. Therefore, these results suggest that L. gasseri MG4247 and L. rhamnosus MG4644 may be used as probiotics to prevent cognitive impairment. Full article
(This article belongs to the Special Issue Oxidative Stress in Brain Function—2nd Edition)
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Review

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28 pages, 1573 KiB  
Review
Oxidative Stress in Brain Function
by Daniela-Marilena Trofin, Dragos-Petrica Sardaru, Dan Trofin, Ilie Onu, Andrei Tutu, Ana Onu, Cristiana Onită, Anca Irina Galaction and Daniela Viorelia Matei
Antioxidants 2025, 14(3), 297; https://doi.org/10.3390/antiox14030297 - 28 Feb 2025
Cited by 1 | Viewed by 1169
Abstract
Oxidative stress (OS) is an important factor in the pathophysiology of numerous neurodegenerative disorders, such as Parkinson’s disease, multiple sclerosis, cerebrovascular pathology or Alzheimer’s disease. OS also significantly influences progression among the various neurodegenerative disorders. The imbalance between the formation of reactive oxygen [...] Read more.
Oxidative stress (OS) is an important factor in the pathophysiology of numerous neurodegenerative disorders, such as Parkinson’s disease, multiple sclerosis, cerebrovascular pathology or Alzheimer’s disease. OS also significantly influences progression among the various neurodegenerative disorders. The imbalance between the formation of reactive oxygen species (ROS) and the body’s capacity to neutralize these toxic byproducts renders the brain susceptible to oxidative injury. Increased amounts of ROS can result in cellular malfunction, apoptosis and neurodegeneration. They also represent a substantial factor in mitochondrial dysfunction, a defining characteristic of neurodegenerative disorders. Comprehending the fundamental mechanisms of OS and its interactions with mitochondrial function, neuroinflammation and cellular protective pathways becomes essential for formulating targeted therapeutics to maintain brain health and reduce the impacts of neurodegeneration. We address recent highlights on the role of OS in brain function in terms of significance for neuronal health and the progression of neurodegenerative disorders. Full article
(This article belongs to the Special Issue Oxidative Stress in Brain Function—2nd Edition)
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