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Transcriptional response to organic compounds from diverse gasoline and biogasoline fuel emissions in human lung cells
H. Libalova, P. Rossner, K. Vrbova, T. Brzicova, J. Sikorova, M. Vojtisek-Lom, V. Beranek, J. Klema, M. Ciganek, J. Neca, M. Machala, J. Topinka,
Language English Country England, Great Britain
Document type Journal Article
- MeSH
- Gasoline analysis toxicity MeSH
- Biofuels analysis toxicity MeSH
- Cell Line MeSH
- Butanols analysis toxicity MeSH
- Ethanol chemistry MeSH
- Transcription, Genetic drug effects MeSH
- Air Pollutants analysis toxicity MeSH
- Humans MeSH
- MAP Kinase Signaling System drug effects MeSH
- Organic Chemicals chemistry toxicity MeSH
- Oxidative Stress drug effects MeSH
- Particulate Matter toxicity MeSH
- Lung drug effects pathology MeSH
- Polycyclic Aromatic Hydrocarbons analysis toxicity MeSH
- DNA Damage MeSH
- Gene Expression Profiling MeSH
- Vehicle Emissions analysis toxicity MeSH
- Inflammation chemically induced pathology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Modern vehicles equipped with Gasoline Direct Injection (GDI) engine have emerged as an important source of particulate emissions potentially harmful to human health. We collected and characterized gasoline exhaust particles (GEPs) produced by neat gasoline fuel (E0) and its blends with 15% ethanol (E15), 25% n-butanol (n-But25) and 25% isobutanol (i-But25). To study the toxic effects of organic compounds extracted from GEPs, we analyzed gene expression profiles in human lung BEAS-2B cells. Despite the lowest GEP mass, n-But25 extract contained the highest concentration of polycyclic aromatic hydrocarbons (PAHs), while i-But25 extract the lowest. Gene expression analysis identified activation of the DNA damage response and other subsequent events (cell cycle arrest, modulation of extracellular matrix, cell adhesion, inhibition of cholesterol biosynthesis) following 4 h exposure to all GEP extracts. The i-But25 extract induced the most distinctive gene expression pattern particularly after 24 h exposure. Whereas E0, E15 and n-But25 extract treatments resulted in persistent stress signaling including DNA damage response, MAPK signaling, oxidative stress, metabolism of PAHs or pro-inflammatory response, i-But25 induced changes related to the metabolism of the cellular nutrients required for cell recovery. Our results indicate that i-But25 extract possessed the weakest genotoxic potency possibly due to the low PAH content.
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- $a Libalova, Helena $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic.
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- $a Transcriptional response to organic compounds from diverse gasoline and biogasoline fuel emissions in human lung cells / $c H. Libalova, P. Rossner, K. Vrbova, T. Brzicova, J. Sikorova, M. Vojtisek-Lom, V. Beranek, J. Klema, M. Ciganek, J. Neca, M. Machala, J. Topinka,
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- $a Modern vehicles equipped with Gasoline Direct Injection (GDI) engine have emerged as an important source of particulate emissions potentially harmful to human health. We collected and characterized gasoline exhaust particles (GEPs) produced by neat gasoline fuel (E0) and its blends with 15% ethanol (E15), 25% n-butanol (n-But25) and 25% isobutanol (i-But25). To study the toxic effects of organic compounds extracted from GEPs, we analyzed gene expression profiles in human lung BEAS-2B cells. Despite the lowest GEP mass, n-But25 extract contained the highest concentration of polycyclic aromatic hydrocarbons (PAHs), while i-But25 extract the lowest. Gene expression analysis identified activation of the DNA damage response and other subsequent events (cell cycle arrest, modulation of extracellular matrix, cell adhesion, inhibition of cholesterol biosynthesis) following 4 h exposure to all GEP extracts. The i-But25 extract induced the most distinctive gene expression pattern particularly after 24 h exposure. Whereas E0, E15 and n-But25 extract treatments resulted in persistent stress signaling including DNA damage response, MAPK signaling, oxidative stress, metabolism of PAHs or pro-inflammatory response, i-But25 induced changes related to the metabolism of the cellular nutrients required for cell recovery. Our results indicate that i-But25 extract possessed the weakest genotoxic potency possibly due to the low PAH content.
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- $a Rossner, Pavel $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic.
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- $a Vrbova, Kristyna $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic.
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- $a Brzicova, Tana $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic; Faculty of Safety Engineering, VSB-Technical University of Ostrava, Lumirova 13, 700 30 Ostrava, Czech Republic.
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- $a Sikorova, Jitka $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic; Institute for Environmental Studies, Faculty of Science, Charles University in Prague, Benatska 2, 128 01 Prague 2, Czech Republic.
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- $a Vojtisek-Lom, Michal $u Center of Vehicles for Sustainable Mobility, Faculty of Mechanical Engineering, Czech Technical University in Prague, Technicka 4, 166 07 Prague, Czech Republic.
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- $a Beranek, Vit $u Center of Vehicles for Sustainable Mobility, Faculty of Mechanical Engineering, Czech Technical University in Prague, Technicka 4, 166 07 Prague, Czech Republic.
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- $a Klema, Jiri $u Department of Cybernetics, Faculty of Electrical Engineering, Czech Technical University in Prague, Karlovo namesti 13, 121 35 Prague, Czech Republic.
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- $a Ciganek, Miroslav $u Department of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 296/70, 621 00 Brno, Czech Republic.
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- $a Neca, Jiri $u Department of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 296/70, 621 00 Brno, Czech Republic.
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- $a Machala, Miroslav $u Department of Chemistry and Toxicology, Veterinary Research Institute, Hudcova 296/70, 621 00 Brno, Czech Republic.
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- $a Topinka, Jan $u Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine AS CR, Videnska 1083, 142 20 Prague, Czech Republic. Electronic address: jtopinka@biomed.cas.cz.
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