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PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes
BACKGROUND: PM(2.5) (aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PM(2.5) exposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increas...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Medknow Publications & Media Pvt Ltd
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5598333/ https://www.ncbi.nlm.nih.gov/pubmed/28816208 http://dx.doi.org/10.4103/0366-6999.212942 |
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author | Hu, Rong Xie, Xiao-Yuan Xu, Si-Ka Wang, Ya-Ning Jiang, Ming Wen, Li-Rong Lai, Wei Guan, Lei |
author_facet | Hu, Rong Xie, Xiao-Yuan Xu, Si-Ka Wang, Ya-Ning Jiang, Ming Wen, Li-Rong Lai, Wei Guan, Lei |
author_sort | Hu, Rong |
collection | PubMed |
description | BACKGROUND: PM(2.5) (aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PM(2.5) exposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increased air PM(2.5) levels and skin disorders although reports on the underlying pathophysiological mechanisms are limited. Oxidative stress is the most common mechanism of PM(2.5)-induced adverse health effects. This study aimed to investigate PM(2.5)-induced oxidative damage and apoptosis in immortalized human keratinocyte (HaCaT) cells. METHODS: HaCaT cells were exposed to 0, 25, 50, 100, or 200 μg/ml PM(2.5) for 24 h. Reactive oxygen species (ROS) generation, lipid peroxidation products, antioxidant activity, DNA damage, apoptotic protein expression, and cell apoptosis were measured. RESULTS: PM(2.5) exposure (0–200 μg/ml) for 24 h resulted in increased ROS levels (arbitrary unit: 201.00 ± 19.28, 264.50 ± 17.91, 305.05 ± 19.57, 427.95 ± 18.32, and 436.70 ± 17.77) and malondialdehyde production (0.54 ± 0.05 nmol/mg prot, 0.61 ± 0.06 nmol/mg prot, 0.68 ± 0.05 nmol/mg prot, 0.70 ± 0.05 nmol/mg prot, and 0.76 ± 0.05 nmol/mg prot), diminished superoxide dismutase activity (6.47 ± 0.28 NU/mg prot, 5.97 ± 0.30 NU/mg prot, 5.15 ± 0.42 NU/mg prot, 4.08 ± 0.20 NU/mg prot, and 3.76 ± 0.37 NU/mg prot), and increased DNA damage and apoptosis in a dose-dependent manner in HaCaT cells. Moreover, cytochrome-c, caspase-3, and caspase-9 expression also increased proportionately with PM(2.5) dosing. CONCLUSION: PM(2.5) might elicit oxidative stress and mitochondria-dependent apoptosis that likely manifests as skin irritation and damage. |
format | Online Article Text |
id | pubmed-5598333 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-55983332017-09-22 PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes Hu, Rong Xie, Xiao-Yuan Xu, Si-Ka Wang, Ya-Ning Jiang, Ming Wen, Li-Rong Lai, Wei Guan, Lei Chin Med J (Engl) Original Article BACKGROUND: PM(2.5) (aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PM(2.5) exposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increased air PM(2.5) levels and skin disorders although reports on the underlying pathophysiological mechanisms are limited. Oxidative stress is the most common mechanism of PM(2.5)-induced adverse health effects. This study aimed to investigate PM(2.5)-induced oxidative damage and apoptosis in immortalized human keratinocyte (HaCaT) cells. METHODS: HaCaT cells were exposed to 0, 25, 50, 100, or 200 μg/ml PM(2.5) for 24 h. Reactive oxygen species (ROS) generation, lipid peroxidation products, antioxidant activity, DNA damage, apoptotic protein expression, and cell apoptosis were measured. RESULTS: PM(2.5) exposure (0–200 μg/ml) for 24 h resulted in increased ROS levels (arbitrary unit: 201.00 ± 19.28, 264.50 ± 17.91, 305.05 ± 19.57, 427.95 ± 18.32, and 436.70 ± 17.77) and malondialdehyde production (0.54 ± 0.05 nmol/mg prot, 0.61 ± 0.06 nmol/mg prot, 0.68 ± 0.05 nmol/mg prot, 0.70 ± 0.05 nmol/mg prot, and 0.76 ± 0.05 nmol/mg prot), diminished superoxide dismutase activity (6.47 ± 0.28 NU/mg prot, 5.97 ± 0.30 NU/mg prot, 5.15 ± 0.42 NU/mg prot, 4.08 ± 0.20 NU/mg prot, and 3.76 ± 0.37 NU/mg prot), and increased DNA damage and apoptosis in a dose-dependent manner in HaCaT cells. Moreover, cytochrome-c, caspase-3, and caspase-9 expression also increased proportionately with PM(2.5) dosing. CONCLUSION: PM(2.5) might elicit oxidative stress and mitochondria-dependent apoptosis that likely manifests as skin irritation and damage. Medknow Publications & Media Pvt Ltd 2017-09-20 /pmc/articles/PMC5598333/ /pubmed/28816208 http://dx.doi.org/10.4103/0366-6999.212942 Text en Copyright: © 2017 Chinese Medical Journal http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. |
spellingShingle | Original Article Hu, Rong Xie, Xiao-Yuan Xu, Si-Ka Wang, Ya-Ning Jiang, Ming Wen, Li-Rong Lai, Wei Guan, Lei PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title | PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title_full | PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title_fullStr | PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title_full_unstemmed | PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title_short | PM(2.5) Exposure Elicits Oxidative Stress Responses and Mitochondrial Apoptosis Pathway Activation in HaCaT Keratinocytes |
title_sort | pm(2.5) exposure elicits oxidative stress responses and mitochondrial apoptosis pathway activation in hacat keratinocytes |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5598333/ https://www.ncbi.nlm.nih.gov/pubmed/28816208 http://dx.doi.org/10.4103/0366-6999.212942 |
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