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Oxidative Stress and Mitochondrial Dysfunction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 1639

Special Issue Editor


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Guest Editor
Department of Biomedical and Biotechnological Sciences (BIOMETEC), University of Catania, 95123 Catania, Italy
Interests: mitochondrial dysfunction; traumatic brain injury, oxidative/nitrosative stress; energy metabolism; neurodegenerations
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Special Issue Information

Dear Colleagues,

Acute (e.g., stroke, traumatic brain injury, etc.) and chronic (e.g., Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, etc.) neurodegenerations are characterized by two profound differences. For the former, the onset of symptoms coincides with the onset of the pathology, with the originating causes, therefore, being known, whilst for the latter, the onset of symptoms is delayed for an unknown period of time with respect to the actual onset of the pathology, with the triggering causes being unknown (or, at the minimum, controversial). Notwithstanding, at the molecular level, acute and chronic neurodegenerations share a number of common pathobiological mechanisms, including oxidative/nitrosative stress, energy penalty, mitochondrial malfunctioning, changes in gene and protein expressions, neuroinflammation, etc. In a large number of cases, the severity of these biochemical/metabolic/molecular alterations is linked to patient outcome (in the case of acute neurodegenerations) and to the progression of the disease (in the case of chronic neurodegenerations).

The aim of this Special Issue is to compile original contributions concerning the interconnections present among the aforementioned pathobiological mechanisms, with special attention paid to oxidative/nitrosative stress and mitochondrial dysfunction in any experimental or clinical model of acute and chronic neurodegenerations. Review article are also welcome, especially if finalized to evaluate the state-of-the-art of potential novel pharmacological approaches.

Prof. Dr. Giuseppe Lazzarino
Guest Editor

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Keywords

  • oxidative/nitrosative stress
  • mitochondrial dysfunction
  • gene and protein expressions
  • neuroinflammation
  • stroke
  • traumatic brain injury
  • Alzheimer’s disease
  • Parkinson’s disease
  • amyotrophic lateral sclerosis
  • multiple sclerosis
  • acute and chronic neurodegenerations

Published Papers (2 papers)

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Research

21 pages, 4156 KiB  
Article
Beta-Hydroxybutyrate Mitigates Sensorimotor and Cognitive Impairments in a Photothrombosis-Induced Ischemic Stroke in Mice
by Artem P. Gureev, Irina S. Sadovnikova, Ekaterina V. Chernyshova, Arina D. Tsvetkova, Polina I. Babenkova, Veronika V. Nesterova, Ekaterina P. Krutskikh, Daria E. Volodina, Natalia A. Samoylova, Nadezda V. Andrianova, Denis N. Silachev and Egor Y. Plotnikov
Int. J. Mol. Sci. 2024, 25(11), 5710; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25115710 - 24 May 2024
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Abstract
The consequences of stroke include cognitive deficits and sensorimotor disturbances, which are largely related to mitochondrial impairments in the brain. In this work, we have shown that the mimetic of the ketogenic diet beta-hydroxybutyrate (βHB) can improve neurological brain function in stroke. At [...] Read more.
The consequences of stroke include cognitive deficits and sensorimotor disturbances, which are largely related to mitochondrial impairments in the brain. In this work, we have shown that the mimetic of the ketogenic diet beta-hydroxybutyrate (βHB) can improve neurological brain function in stroke. At 3 weeks after photothrombotic stroke, mice receiving βHB with drinking water before and after surgery recovered faster in terms of sensorimotor functions assessed by the string test and static rods and cognitive functions assessed by the Morris water maze. At the same time, the βHB-treated mice had lower expression of some markers of astrocyte activation and inflammation (Gfap, Il-1b, Tnf). We hypothesize that long-term administration of βHB promotes the activation of the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) pathway, which leads to increased expression of antioxidant genes targeting mitochondria and genes involved in signaling pathways necessary for the maintenance of synaptic plasticity. βHB partially maintained mitochondrial DNA (mtDNA) integrity during the first days after photothrombosis. However, in the following three weeks, the number of mtDNA damages increased in all experimental groups, which coincided with a decrease in Ogg1 expression, which plays an important role in mtDNA repair. Thus, we can assume that βHB is not only an important metabolite that provides additional energy to brain tissue during recovery from stroke under conditions of mitochondrial damage but also an important signaling molecule that supports neuronal plasticity and reduces neuroinflammation. Full article
(This article belongs to the Special Issue Oxidative Stress and Mitochondrial Dysfunction)
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13 pages, 1873 KiB  
Article
The WMI Rat of Premature Cognitive Aging Presents Intrinsic Vulnerability to Oxidative Stress in Primary Neurons and Astrocytes Compared to Its Nearly Isogenic WLI Control
by Adriana Ferreira, Aspen Harter, Sana Afreen, Karoly Kanai, Sandor Batori and Eva E. Redei
Int. J. Mol. Sci. 2024, 25(3), 1692; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25031692 - 30 Jan 2024
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Abstract
The primary neuronal and astrocyte culture described here is from the stress-hyperreactive Wistar Kyoto (WKY) More Immobile (WMI) rat with premature aging-related memory deficit, and its nearly isogenic control, the Less Immobile (WLI) strain. Primary WMI hippocampal neurons and cortical astrocytes are significantly [...] Read more.
The primary neuronal and astrocyte culture described here is from the stress-hyperreactive Wistar Kyoto (WKY) More Immobile (WMI) rat with premature aging-related memory deficit, and its nearly isogenic control, the Less Immobile (WLI) strain. Primary WMI hippocampal neurons and cortical astrocytes are significantly more sensitive to oxidative stress (OS) generated by administration of H2O2 compared to WLI cells as measured by the trypan blue cell viability assay. Intrinsic genetic vulnerability is also suggested by the decreased gene expression in WMI neurons of catalase (Cat), and in WMI cortical astrocytes of insulin-like growth factor 2 (Igf2), synuclein gamma (Sncg) and glutathione peroxidase 2 (Gpx2) compared to WLI. The expressions of several mitochondrial genes are dramatically increased in response to H2O2 treatment in WLI, but not in WMI cortical astrocytes. We propose that the vulnerability of WMI neurons to OS is due to the genetic differences between the WLI and WMI. Furthermore, the upregulation of mitochondrial genes may be a compensatory response to the generation of free radicals by OS in the WLIs, and this mechanism is disturbed in the WMIs. Thus, this pilot study suggests intrinsic vulnerabilities in the WMI hippocampal neurons and cortical astrocytes, and affirm the efficacy of this bimodal in vitro screening system for finding novel drug targets to prevent oxidative damage in illnesses. Full article
(This article belongs to the Special Issue Oxidative Stress and Mitochondrial Dysfunction)
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