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Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression

Chronic fine particulate matter (PM(2.5)) exposure causes oxidative stress and leads to many diseases in human like respiratory and cardiovascular disorders, and lung cancer. It is known that toxic responses elicited by PM(2.5) particles depend on its physical and chemical characteristics that are g...

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Detalles Bibliográficos
Autores principales: Veerappan, Indhumathi, Sankareswaran, Senthil Kumar, Palanisamy, Rajaguru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651735/
https://www.ncbi.nlm.nih.gov/pubmed/31284452
http://dx.doi.org/10.3390/ijerph16132389
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author Veerappan, Indhumathi
Sankareswaran, Senthil Kumar
Palanisamy, Rajaguru
author_facet Veerappan, Indhumathi
Sankareswaran, Senthil Kumar
Palanisamy, Rajaguru
author_sort Veerappan, Indhumathi
collection PubMed
description Chronic fine particulate matter (PM(2.5)) exposure causes oxidative stress and leads to many diseases in human like respiratory and cardiovascular disorders, and lung cancer. It is known that toxic responses elicited by PM(2.5) particles depend on its physical and chemical characteristics that are greatly influenced by the source. Dietary polyphenolic compounds that possess antioxidant and free radical scavenging properties could be used for therapeutic or preventive approaches against air pollution related health hazards. This study evaluates characteristics and toxicity of PM(2.5) collected from rural, urban, industrial, and traffic regions in and around Coimbatore City, Tamilnadu, India. Traffic PM(2.5) particles contained higher amounts of metals and polycyclic aromatic hydrocarbons (PAHs). It also possessed higher levels of oxidative potential, induced more intracellular reactive oxygen species (ROS), and caused more levels of cell death and DNA damage in human respiratory cells. Its exposure up regulated DNA damage response related miR222, miR210, miR101, miR34a, and miR93 and MycN and suppressed Rad52. Pre-treatment with morin significantly decreased the PM(2.5) induced toxicity and conferred protection against PM(2.5) induced altered miRNA expression. Results of this study showed that cytoprotective effect of morin is due to its antioxidative and free radical scavenging activity.
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spelling pubmed-66517352019-08-08 Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression Veerappan, Indhumathi Sankareswaran, Senthil Kumar Palanisamy, Rajaguru Int J Environ Res Public Health Article Chronic fine particulate matter (PM(2.5)) exposure causes oxidative stress and leads to many diseases in human like respiratory and cardiovascular disorders, and lung cancer. It is known that toxic responses elicited by PM(2.5) particles depend on its physical and chemical characteristics that are greatly influenced by the source. Dietary polyphenolic compounds that possess antioxidant and free radical scavenging properties could be used for therapeutic or preventive approaches against air pollution related health hazards. This study evaluates characteristics and toxicity of PM(2.5) collected from rural, urban, industrial, and traffic regions in and around Coimbatore City, Tamilnadu, India. Traffic PM(2.5) particles contained higher amounts of metals and polycyclic aromatic hydrocarbons (PAHs). It also possessed higher levels of oxidative potential, induced more intracellular reactive oxygen species (ROS), and caused more levels of cell death and DNA damage in human respiratory cells. Its exposure up regulated DNA damage response related miR222, miR210, miR101, miR34a, and miR93 and MycN and suppressed Rad52. Pre-treatment with morin significantly decreased the PM(2.5) induced toxicity and conferred protection against PM(2.5) induced altered miRNA expression. Results of this study showed that cytoprotective effect of morin is due to its antioxidative and free radical scavenging activity. MDPI 2019-07-05 2019-07 /pmc/articles/PMC6651735/ /pubmed/31284452 http://dx.doi.org/10.3390/ijerph16132389 Text en © 2019 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
Veerappan, Indhumathi
Sankareswaran, Senthil Kumar
Palanisamy, Rajaguru
Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title_full Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title_fullStr Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title_full_unstemmed Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title_short Morin Protects Human Respiratory Cells from PM(2.5) Induced Genotoxicity by Mitigating ROS and Reverting Altered miRNA Expression
title_sort morin protects human respiratory cells from pm(2.5) induced genotoxicity by mitigating ros and reverting altered mirna expression
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651735/
https://www.ncbi.nlm.nih.gov/pubmed/31284452
http://dx.doi.org/10.3390/ijerph16132389
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