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New Insights into Neurotoxicity

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: 31 July 2024 | Viewed by 1221

Special Issue Editor


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Guest Editor
Department of Biosciences, Durham University, Durham DH1 3LE, UK
Interests: ER stress; oxidative stress; inflammation; senescence; autophagy; proteinopathies; metallopathies; channelopathies; chronic; neuroglia; vascular
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Special Issue Information

Dear Colleagues,

Neurotoxicity occurs when the exposure to natural or artificial toxic substances (termed neurotoxicants) alters the normal activity of the nervous system. This can eventually stress or potentially kill neurons crucial for transmitting and processing signals in the brain and other parts of the nervous system. Examples of neurotoxic agents include chemotherapy drugs that are used to kill rapidly growing cells, drug therapies or drugs of abuse, certain foods and food additives, insecticides/pesticides, cosmetics, radiation, industrial and cleaning solvents, and heavy metals such as vanadium, chromium, mercury and lead. For example, heavy metal accumulation increases the brain’s vulnerability to neurotoxic shocks through mechanisms such mitochondrial failure, calcium-ion dyshomeostasis in neurons and glia, an accumulation of damaged proteins, reduced DNA repair, decreased neurogenesis and impaired energy metabolism. Alongside causing cognitive deterioration and dysfunction of the autonomic nervous system, neurotoxicity has also been shown to be a major contributor to progressive neurological disorders such as Alzheimer’s and Parkinson’s diseases. This Special Issue will explore “New Insights into Neurotoxicity”, and how it influences the aging process and tips normal aging into a disease state, as well as new approaches to provide neuroprotection, neuroplasticity and neurorepair.

Dr. Paul L. Chazot
Guest Editor

Manuscript Submission Information

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Keywords

  • neurotoxicity
  • neurotoxicants
  • nervous system
  • heavy metal

Published Papers (1 paper)

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Research

23 pages, 7526 KiB  
Article
Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist
by Amany Digal Ladagu, Funmilayo Eniola Olopade, Paul Chazot, Ademola A. Oyagbemi, Samuel Ohiomokhare, Oluwabusayo Racheal Folarin, Taidinda Tashara Gilbert, Madison Fuller, Toan Luong, Adeboye Adejare and James O. Olopade
Int. J. Mol. Sci. 2023, 24(23), 16710; https://doi.org/10.3390/ijms242316710 - 24 Nov 2023
Viewed by 1084
Abstract
Exposure to heavy metals, such as vanadium, poses an ongoing environmental and health threat, heightening the risk of neurodegenerative disorders. While several compounds have shown promise in mitigating vanadium toxicity, their efficacy is limited. Effective strategies involve targeting specific subunits of the NMDA [...] Read more.
Exposure to heavy metals, such as vanadium, poses an ongoing environmental and health threat, heightening the risk of neurodegenerative disorders. While several compounds have shown promise in mitigating vanadium toxicity, their efficacy is limited. Effective strategies involve targeting specific subunits of the NMDA receptor, a glutamate receptor linked to neurodegenerative conditions. The potential neuroprotective effects of ZA-II-05, an NMDA receptor antagonist, against vanadium-induced neurotoxicity were explored in this study. Organotypic rat hippocampal slices, and live mice, were used as models to comprehensively evaluate the compound’s impact. Targeted in vivo fluorescence analyses of the hippocampal slices using propidium iodide as a marker for cell death was utilized. The in vivo study involved five dams, each with eight pups, which were randomly assigned to five experimental groups (n = 8 pups). After administering treatments intraperitoneally over six months, various brain regions were assessed for neuropathologies using different immunohistochemical markers. High fluorescence intensity was observed in the hippocampal slices treated with vanadium, signifying cell death. Vanadium-exposed mice exhibited demyelination, microgliosis, and neuronal cell loss. Significantly, treatment with ZA-II-05 resulted in reduced cellular death in the rat hippocampal slices and preserved cellular integrity and morphological architecture in different anatomical regions, suggesting its potential in countering vanadium-induced neurotoxicity. Full article
(This article belongs to the Special Issue New Insights into Neurotoxicity)
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