Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.

Acrolein is a ubiquitous pollutant abundant in cigarette smoke, mobile exhaust, and industrial waste. There is limited literature on the effects of acrolein on vocal fold tissue, although there are clinical reports of voice changes after pollutant exposures. Vocal folds are responsible for voice pro...

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Main Authors: Xinxin Liu, Wei Zheng, M Preeti Sivasankar
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5028054?pdf=render
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spelling doaj-d8cce9e7dced4662a3d1edaf280b02492020-11-25T00:04:27ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01119e016323710.1371/journal.pone.0163237Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.Xinxin LiuWei ZhengM Preeti SivasankarAcrolein is a ubiquitous pollutant abundant in cigarette smoke, mobile exhaust, and industrial waste. There is limited literature on the effects of acrolein on vocal fold tissue, although there are clinical reports of voice changes after pollutant exposures. Vocal folds are responsible for voice production. The overall objective of this study was to investigate the effects of acrolein exposure on viable, excised vocal fold epithelial tissue and to characterize the mechanism underlying acrolein toxicity. Vocal fold epithelia were studied because they form the outermost layer of the vocal folds and are a primary recipient of inhaled pollutants. Porcine vocal fold epithelia were exposed to 0, 50, 100, 500, 900 or 1300 μM of acrolein for 3 hours; the metabolic activity, epithelial resistance, epithelial permeability, tight junction protein (occludin and claudin 3) expression, cell membrane integrity and lipid peroxidation were investigated. The data demonstrated that acrolein exposure at 500 μM significantly reduced vocal fold epithelial metabolic activity by 27.2% (p≤0.001). Incubation with 100 μM acrolein caused a marked increase in epithelial permeability by 130.5% (p<0.05) and a reduction in transepithelial electrical resistance (TEER) by 180.0% (p<0.001). While the expression of tight junctional protein did not change in acrolein-treated samples, the cell membrane integrity was significantly damaged with a 45.6% increase of lipid peroxidation as compared to controls (p<0.05). Taken together, these data provide evidence that acute acrolein exposure impairs vocal fold epithelial barrier integrity. Lipid peroxidation-induced cell membrane damage may play an important role in reducing the barrier function of the epithelium.http://europepmc.org/articles/PMC5028054?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Xinxin Liu
Wei Zheng
M Preeti Sivasankar
spellingShingle Xinxin Liu
Wei Zheng
M Preeti Sivasankar
Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
PLoS ONE
author_facet Xinxin Liu
Wei Zheng
M Preeti Sivasankar
author_sort Xinxin Liu
title Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
title_short Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
title_full Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
title_fullStr Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
title_full_unstemmed Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.
title_sort acute acrolein exposure induces impairment of vocal fold epithelial barrier function.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2016-01-01
description Acrolein is a ubiquitous pollutant abundant in cigarette smoke, mobile exhaust, and industrial waste. There is limited literature on the effects of acrolein on vocal fold tissue, although there are clinical reports of voice changes after pollutant exposures. Vocal folds are responsible for voice production. The overall objective of this study was to investigate the effects of acrolein exposure on viable, excised vocal fold epithelial tissue and to characterize the mechanism underlying acrolein toxicity. Vocal fold epithelia were studied because they form the outermost layer of the vocal folds and are a primary recipient of inhaled pollutants. Porcine vocal fold epithelia were exposed to 0, 50, 100, 500, 900 or 1300 μM of acrolein for 3 hours; the metabolic activity, epithelial resistance, epithelial permeability, tight junction protein (occludin and claudin 3) expression, cell membrane integrity and lipid peroxidation were investigated. The data demonstrated that acrolein exposure at 500 μM significantly reduced vocal fold epithelial metabolic activity by 27.2% (p≤0.001). Incubation with 100 μM acrolein caused a marked increase in epithelial permeability by 130.5% (p<0.05) and a reduction in transepithelial electrical resistance (TEER) by 180.0% (p<0.001). While the expression of tight junctional protein did not change in acrolein-treated samples, the cell membrane integrity was significantly damaged with a 45.6% increase of lipid peroxidation as compared to controls (p<0.05). Taken together, these data provide evidence that acute acrolein exposure impairs vocal fold epithelial barrier integrity. Lipid peroxidation-induced cell membrane damage may play an important role in reducing the barrier function of the epithelium.
url http://europepmc.org/articles/PMC5028054?pdf=render
work_keys_str_mv AT xinxinliu acuteacroleinexposureinducesimpairmentofvocalfoldepithelialbarrierfunction
AT weizheng acuteacroleinexposureinducesimpairmentofvocalfoldepithelialbarrierfunction
AT mpreetisivasankar acuteacroleinexposureinducesimpairmentofvocalfoldepithelialbarrierfunction
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