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Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, gi...

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Autores principales: Cheng, Hong, Yang, Bobo, Ke, Tao, Li, Shaojun, Yang, Xiaobo, Aschner, Michael, Chen, Pan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8235163/
https://www.ncbi.nlm.nih.gov/pubmed/34204190
http://dx.doi.org/10.3390/toxics9060142
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author Cheng, Hong
Yang, Bobo
Ke, Tao
Li, Shaojun
Yang, Xiaobo
Aschner, Michael
Chen, Pan
author_facet Cheng, Hong
Yang, Bobo
Ke, Tao
Li, Shaojun
Yang, Xiaobo
Aschner, Michael
Chen, Pan
author_sort Cheng, Hong
collection PubMed
description Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.
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spelling pubmed-82351632021-06-27 Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders Cheng, Hong Yang, Bobo Ke, Tao Li, Shaojun Yang, Xiaobo Aschner, Michael Chen, Pan Toxics Review Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system. MDPI 2021-06-17 /pmc/articles/PMC8235163/ /pubmed/34204190 http://dx.doi.org/10.3390/toxics9060142 Text en © 2021 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
Cheng, Hong
Yang, Bobo
Ke, Tao
Li, Shaojun
Yang, Xiaobo
Aschner, Michael
Chen, Pan
Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title_full Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title_fullStr Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title_full_unstemmed Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title_short Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders
title_sort mechanisms of metal-induced mitochondrial dysfunction in neurological disorders
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8235163/
https://www.ncbi.nlm.nih.gov/pubmed/34204190
http://dx.doi.org/10.3390/toxics9060142
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