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Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset
In northern Italy, biomass burning-derived (BB) particles and diesel exhaust particles (DEP) are considered the most significant contributors to ultrafine particle (UFP) emission. However, a comparison between their impact on different brain regions was not investigated until now. Therefore, male BA...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279458/ https://www.ncbi.nlm.nih.gov/pubmed/32456361 http://dx.doi.org/10.3390/ijms21103699 |
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author | Milani, Chiara Farina, Francesca Botto, Laura Massimino, Luca Lonati, Elena Donzelli, Elisabetta Ballarini, Elisa Crippa, Luca Marmiroli, Paola Bulbarelli, Alessandra Palestini, Paola |
author_facet | Milani, Chiara Farina, Francesca Botto, Laura Massimino, Luca Lonati, Elena Donzelli, Elisabetta Ballarini, Elisa Crippa, Luca Marmiroli, Paola Bulbarelli, Alessandra Palestini, Paola |
author_sort | Milani, Chiara |
collection | PubMed |
description | In northern Italy, biomass burning-derived (BB) particles and diesel exhaust particles (DEP) are considered the most significant contributors to ultrafine particle (UFP) emission. However, a comparison between their impact on different brain regions was not investigated until now. Therefore, male BALB/c mice were treated with a single or three consecutive intratracheal instillations using 50 µg of UFPs in 100 µL of isotonic saline solution or 100 µL of isotonic saline solution alone, and brains were collected and analyzed. Proteins related to oxidative stress and inflammation, as well as Alzheimer’s disease markers, were examined in the hippocampus, cerebellum, and the rest of the brain (RoB). Histopathological examination of the brain was also performed. Moreover, correlations among different brain, pulmonary, and cardiovascular markers were performed, allowing us to identify the potentially most stressful UFP source. Although both acute exposures induced inflammatory pathways in mouse brain, only DEP showed strong oxidative stress. The sub-acute exposure also induced the modulation of APP and BACE1 protein levels for both UFPs. We observed that DEP exposure is more harmful than BB, and this different response could be explained by this UFP’s different chemical composition and reactivity. |
format | Online Article Text |
id | pubmed-7279458 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72794582020-06-17 Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset Milani, Chiara Farina, Francesca Botto, Laura Massimino, Luca Lonati, Elena Donzelli, Elisabetta Ballarini, Elisa Crippa, Luca Marmiroli, Paola Bulbarelli, Alessandra Palestini, Paola Int J Mol Sci Article In northern Italy, biomass burning-derived (BB) particles and diesel exhaust particles (DEP) are considered the most significant contributors to ultrafine particle (UFP) emission. However, a comparison between their impact on different brain regions was not investigated until now. Therefore, male BALB/c mice were treated with a single or three consecutive intratracheal instillations using 50 µg of UFPs in 100 µL of isotonic saline solution or 100 µL of isotonic saline solution alone, and brains were collected and analyzed. Proteins related to oxidative stress and inflammation, as well as Alzheimer’s disease markers, were examined in the hippocampus, cerebellum, and the rest of the brain (RoB). Histopathological examination of the brain was also performed. Moreover, correlations among different brain, pulmonary, and cardiovascular markers were performed, allowing us to identify the potentially most stressful UFP source. Although both acute exposures induced inflammatory pathways in mouse brain, only DEP showed strong oxidative stress. The sub-acute exposure also induced the modulation of APP and BACE1 protein levels for both UFPs. We observed that DEP exposure is more harmful than BB, and this different response could be explained by this UFP’s different chemical composition and reactivity. MDPI 2020-05-24 /pmc/articles/PMC7279458/ /pubmed/32456361 http://dx.doi.org/10.3390/ijms21103699 Text en © 2020 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Milani, Chiara Farina, Francesca Botto, Laura Massimino, Luca Lonati, Elena Donzelli, Elisabetta Ballarini, Elisa Crippa, Luca Marmiroli, Paola Bulbarelli, Alessandra Palestini, Paola Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title | Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title_full | Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title_fullStr | Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title_full_unstemmed | Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title_short | Systemic Exposure to Air Pollution Induces Oxidative Stress and Inflammation in Mouse Brain, Contributing to Neurodegeneration Onset |
title_sort | systemic exposure to air pollution induces oxidative stress and inflammation in mouse brain, contributing to neurodegeneration onset |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7279458/ https://www.ncbi.nlm.nih.gov/pubmed/32456361 http://dx.doi.org/10.3390/ijms21103699 |
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