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Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity

Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions, including differences in the characteristics of tissues and cells, exposure age (fetal, childhood, or adulthood), and exposure levels. R...

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Detalles Bibliográficos
Autores principales: Fujimura, Masatake, Usuki, Fusako
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9266708/
https://www.ncbi.nlm.nih.gov/pubmed/35806222
http://dx.doi.org/10.3390/ijms23137218
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author Fujimura, Masatake
Usuki, Fusako
author_facet Fujimura, Masatake
Usuki, Fusako
author_sort Fujimura, Masatake
collection PubMed
description Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions, including differences in the characteristics of tissues and cells, exposure age (fetal, childhood, or adulthood), and exposure levels. Research has highlighted the importance of oxidative stress in the pathogenesis of MeHg-induced toxicity and the site- and cell-specific nature of MeHg-induced neurotoxicity. The cerebellar granule cells and deeper layer cerebrocortical neurons are vulnerable to MeHg. In contrast, the hippocampal neurons are resistant to MeHg, even at high mercury accumulation levels. This review summarizes the mechanisms underlying MeHg-mediated intracellular events that lead to site-specific neurotoxicity. Specifically, we discuss the mechanisms associated with the redox ability, neural outgrowth and synapse formation, cellular signaling pathways, epigenetics, and the inflammatory conditions of microglia.
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spelling pubmed-92667082022-07-09 Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity Fujimura, Masatake Usuki, Fusako Int J Mol Sci Review Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions, including differences in the characteristics of tissues and cells, exposure age (fetal, childhood, or adulthood), and exposure levels. Research has highlighted the importance of oxidative stress in the pathogenesis of MeHg-induced toxicity and the site- and cell-specific nature of MeHg-induced neurotoxicity. The cerebellar granule cells and deeper layer cerebrocortical neurons are vulnerable to MeHg. In contrast, the hippocampal neurons are resistant to MeHg, even at high mercury accumulation levels. This review summarizes the mechanisms underlying MeHg-mediated intracellular events that lead to site-specific neurotoxicity. Specifically, we discuss the mechanisms associated with the redox ability, neural outgrowth and synapse formation, cellular signaling pathways, epigenetics, and the inflammatory conditions of microglia. MDPI 2022-06-29 /pmc/articles/PMC9266708/ /pubmed/35806222 http://dx.doi.org/10.3390/ijms23137218 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Fujimura, Masatake
Usuki, Fusako
Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title_full Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title_fullStr Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title_full_unstemmed Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title_short Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity
title_sort cellular conditions responsible for methylmercury-mediated neurotoxicity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9266708/
https://www.ncbi.nlm.nih.gov/pubmed/35806222
http://dx.doi.org/10.3390/ijms23137218
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