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The Biological Effects of Complete Gasoline Engine Emissions Exposure in a 3D Human Airway Model (MucilAirTM) and in Human Bronchial Epithelial Cells (BEAS-2B)
P. Rossner, T. Cervena, M. Vojtisek-Lom, K. Vrbova, A. Ambroz, Z. Novakova, F. Elzeinova, H. Margaryan, V. Beranek, M. Pechout, D. Macoun, J. Klema, A. Rossnerova, M. Ciganek, J. Topinka,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
18-04719S
Grantová Agentura České Republiky
NLK
Directory of Open Access Journals
od 2000
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
PubMed Central
od 2007
Europe PubMed Central
od 2007
ProQuest Central
od 2000-03-01
Open Access Digital Library
od 2000-01-01
Open Access Digital Library
od 2007-01-01
Health & Medicine (ProQuest)
od 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
PubMed
31739528
DOI
10.3390/ijms20225710
Knihovny.cz E-zdroje
- MeSH
- biologické markery MeSH
- biologické modely * MeSH
- elektrická impedance MeSH
- epitelové buňky účinky léků metabolismus MeSH
- exprese genu MeSH
- lidé MeSH
- muciny biosyntéza MeSH
- respirační sliznice účinky léků metabolismus MeSH
- výfukové emise vozidel toxicita MeSH
- vystavení vlivu životního prostředí škodlivé účinky MeSH
- zlomy DNA MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAirTM) and in human bronchial epithelial cells (BEAS-2B) grown at the air-liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures; DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAirTM. There were no effects of this kind observed in BEAS-2B cells; in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model.
Department of Chemistry and Toxicology Veterinary Research Institute 621 00 Brno Czech Republic
Department of Computer Science Czech Technical University Prague 12135 Prague Czech Republic
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- $a The Biological Effects of Complete Gasoline Engine Emissions Exposure in a 3D Human Airway Model (MucilAirTM) and in Human Bronchial Epithelial Cells (BEAS-2B) / $c P. Rossner, T. Cervena, M. Vojtisek-Lom, K. Vrbova, A. Ambroz, Z. Novakova, F. Elzeinova, H. Margaryan, V. Beranek, M. Pechout, D. Macoun, J. Klema, A. Rossnerova, M. Ciganek, J. Topinka,
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- $a The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAirTM) and in human bronchial epithelial cells (BEAS-2B) grown at the air-liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures; DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAirTM. There were no effects of this kind observed in BEAS-2B cells; in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model.
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