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Mitochondrial Dysfunction as a Hallmark of Environmental Injury
Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular and molecular events triggered by an exposure to environmental pollutants are extremely variable and depend on the age, the chronicity and the doses of exposu...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750015/ https://www.ncbi.nlm.nih.gov/pubmed/35011671 http://dx.doi.org/10.3390/cells11010110 |
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author | Duarte-Hospital, Carolina Tête, Arnaud Brial, François Benoit, Louise Koual, Meriem Tomkiewicz, Céline Kim, Min Ji Blanc, Etienne B. Coumoul, Xavier Bortoli, Sylvie |
author_facet | Duarte-Hospital, Carolina Tête, Arnaud Brial, François Benoit, Louise Koual, Meriem Tomkiewicz, Céline Kim, Min Ji Blanc, Etienne B. Coumoul, Xavier Bortoli, Sylvie |
author_sort | Duarte-Hospital, Carolina |
collection | PubMed |
description | Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular and molecular events triggered by an exposure to environmental pollutants are extremely variable and depend on the age, the chronicity and the doses of exposure. Only a fraction of all relevant mechanisms involved in the onset and progression of pathologies in response to toxicants has probably been identified. Mitochondria are central hubs of metabolic and cell signaling responsible for a large variety of biochemical processes, including oxidative stress, metabolite production, energy transduction, hormone synthesis, and apoptosis. Growing evidence highlights mitochondrial dysfunction as a major hallmark of environmental insults. Here, we present mitochondria as crucial organelles for healthy metabolic homeostasis and whose dysfunction induces critical adverse effects. Then, we review the multiple mechanisms of action of pollutants causing mitochondrial toxicity in link with chronic diseases. We propose the Aryl hydrocarbon Receptor (AhR) as a model of “exposome receptor”, whose activation by environmental pollutants leads to various toxic events through mitochondrial dysfunction. Finally, we provide some remarks related to mitotoxicity and risk assessment. |
format | Online Article Text |
id | pubmed-8750015 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-87500152022-01-12 Mitochondrial Dysfunction as a Hallmark of Environmental Injury Duarte-Hospital, Carolina Tête, Arnaud Brial, François Benoit, Louise Koual, Meriem Tomkiewicz, Céline Kim, Min Ji Blanc, Etienne B. Coumoul, Xavier Bortoli, Sylvie Cells Review Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular and molecular events triggered by an exposure to environmental pollutants are extremely variable and depend on the age, the chronicity and the doses of exposure. Only a fraction of all relevant mechanisms involved in the onset and progression of pathologies in response to toxicants has probably been identified. Mitochondria are central hubs of metabolic and cell signaling responsible for a large variety of biochemical processes, including oxidative stress, metabolite production, energy transduction, hormone synthesis, and apoptosis. Growing evidence highlights mitochondrial dysfunction as a major hallmark of environmental insults. Here, we present mitochondria as crucial organelles for healthy metabolic homeostasis and whose dysfunction induces critical adverse effects. Then, we review the multiple mechanisms of action of pollutants causing mitochondrial toxicity in link with chronic diseases. We propose the Aryl hydrocarbon Receptor (AhR) as a model of “exposome receptor”, whose activation by environmental pollutants leads to various toxic events through mitochondrial dysfunction. Finally, we provide some remarks related to mitotoxicity and risk assessment. MDPI 2021-12-30 /pmc/articles/PMC8750015/ /pubmed/35011671 http://dx.doi.org/10.3390/cells11010110 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 Duarte-Hospital, Carolina Tête, Arnaud Brial, François Benoit, Louise Koual, Meriem Tomkiewicz, Céline Kim, Min Ji Blanc, Etienne B. Coumoul, Xavier Bortoli, Sylvie Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title | Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title_full | Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title_fullStr | Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title_full_unstemmed | Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title_short | Mitochondrial Dysfunction as a Hallmark of Environmental Injury |
title_sort | mitochondrial dysfunction as a hallmark of environmental injury |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750015/ https://www.ncbi.nlm.nih.gov/pubmed/35011671 http://dx.doi.org/10.3390/cells11010110 |
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