The Genotoxicity of Organic Extracts from Particulate Emissions Produced by Neat Gasoline (E0) and a Gasoline-Ethanol Blend (E15) in BEAS-2B Cells
Status PubMed-not-MEDLINE Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
Grantová podpora
18-06548Y
Czech Science Foundation
LM2018124
Ministry of Education Youth and Sports
LM2023053
Ministry of Education Youth and Sports
CZ.02.1.01/0.0/0.0/16_013/0001821
Ministry of Education Youth and Sports
PubMed
38535490
PubMed Central
PMC10970876
DOI
10.3390/jox14010001
PII: jox14010001
Knihovny.cz E-zdroje
- Klíčová slova
- alternative fuels, gasoline particulate emissions, genotoxicity, human pulmonary cell line, organic PM extracts, polycyclic aromatic hydrocarbons,
- Publikační typ
- časopisecké články MeSH
Emissions from modern gasoline engines represent an environmental and health risk. In this study, we aimed to compare the toxicity of organic compound mixtures extracted from particulate matter (PM extracts) produced by neat gasoline (E0) and a blend containing 15% ethanol (E15), which is offered as an alternative to non-renewable fossil fuels. Human lung BEAS-2B cells were exposed to PM extracts, and biomarkers of genotoxicity, such as DNA damage evaluated by comet assay, micronuclei formation, levels of phosphorylated histone H2AX, the expression of genes relevant to the DNA damage response, and exposure to polycyclic aromatic hydrocarbons (PAHs), were determined. Results showed that both PM extracts significantly increased the level of oxidized DNA lesions. The E0 extract exhibited a more pronounced effect, possibly due to the higher content of nitrated PAHs. Other endpoints were not substantially affected by any of the PM extracts. Gene expression analysis revealed mild but coordinated induction of genes related to DNA damage response, and a strong induction of PAH-inducible genes, indicating activation of the aryl hydrocarbon receptor (AhR). Our data suggest that the addition of ethanol into the gasoline diminished the oxidative DNA damage, but no effect on other genotoxicity biomarkers was observed. Activated AhR may play an important role in the toxicity of gasoline PM emissions.
Zobrazit více v PubMed
Englert N. Fine Particles and Human Health—A Review of Epidemiological Studies. Toxicol. Lett. 2004;149:235–242. doi: 10.1016/j.toxlet.2003.12.035. PubMed DOI
Xia T., Zhu Y., Mu L., Zhang Z.-F., Liu S. Pulmonary Diseases Induced by Ambient Ultrafine and Engineered Nanoparticles in Twenty-First Century. Natl. Sci. Rev. 2016;3:416–429. doi: 10.1093/nsr/nww064. PubMed DOI PMC
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans . IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 92. International Agency for Research on Cancer; Lyon, France: 2010. Some Non-Heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures; pp. 1–853. PubMed PMC
Xue W., Warshawsky D. Metabolic Activation of Polycyclic and Heterocyclic Aromatic Hydrocarbons and DNA Damage: A Review. Toxicol. Appl. Pharmacol. 2005;206:73–93. doi: 10.1016/j.taap.2004.11.006. PubMed DOI
Vione D., Barra S., De Gennaro G., De Rienzo M., Gilardoni S., Perrone M.G., Pozzoli L. Polycyclic Aromatic Hydrocarbons in the Atmosphere: Monitoring, Sources, Sinks and Fate. II: Sinks and Fate. Ann. Chim. 2004;94:257–268. doi: 10.1002/adic.200490031. PubMed DOI
Park M., Joo H.S., Lee K., Jang M., Kim S.D., Kim I., Borlaza L.J.S., Lim H., Shin H., Chung K.H., et al. Differential Toxicities of Fine Particulate Matters from Various Sources. Sci. Rep. 2018;8:17007. doi: 10.1038/s41598-018-35398-0. PubMed DOI PMC
Platt S.M., El Haddad I., Pieber S.M., Zardini A.A., Suarez-Bertoa R., Clairotte M., Daellenbach K.R., Huang R.-J., Slowik J.G., Hellebust S., et al. Gasoline Cars Produce More Carbonaceous Particulate Matter than Modern Filter-Equipped Diesel Cars. Sci. Rep. 2017;7:4926. doi: 10.1038/s41598-017-03714-9. PubMed DOI PMC
International Agency for Research on Cancer . Diesel and Gasoline Engine Exhaust and Some Nitroarenes. International Agency for Research on Cancer; Lyon, France: 2012.
Muñoz M., Heeb N.V., Haag R., Honegger P., Zeyer K., Mohn J., Comte P., Czerwinski J. Bioethanol Blending Reduces Nanoparticle, PAH, and Alkyl- and Nitro-PAH Emissions and the Genotoxic Potential of Exhaust from a Gasoline Direct Injection Flex-Fuel Vehicle. Environ. Sci. Technol. 2016;50:11853–11861. doi: 10.1021/acs.est.6b02606. PubMed DOI
Karavalakis G., Durbin T.D., Shrivastava M., Zheng Z., Villela M., Jung H. Impacts of Ethanol Fuel Level on Emissions of Regulated and Unregulated Pollutants from a Fleet of Gasoline Light-Duty Vehicles. Fuel. 2012;93:549–558. doi: 10.1016/j.fuel.2011.09.021. DOI
Libalova H., Rossner P., Vrbova K., Brzicova T., Sikorova J., Vojtisek-Lom M., Beranek V., Klema J., Ciganek M., Neca J., et al. Transcriptional Response to Organic Compounds from Diverse Gasoline and Biogasoline Fuel Emissions in Human Lung Cells. Toxicol. Vitr. 2018;48:329–341. doi: 10.1016/j.tiv.2018.02.002. PubMed DOI
Novotná B., Sikorová J., Milcová A., Pechout M., Dittrich L., Vojtíšek-Lom M., Rossner P.J., Brzicová T., Topinka J. The Genotoxicity of Organic Extracts from Particulate Truck Emissions Produced at Various Engine Operating Modes Using Diesel or Biodiesel (B100) Fuel: A Pilot Study. Mutat. Res. Genet. Toxicol. Environ. Mutagen. 2019;845:403034. doi: 10.1016/j.mrgentox.2019.03.007. PubMed DOI
Livak K.J., Schmittgen T.D. Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2-ΔΔCT Method. Methods. 2001;25:402–408. doi: 10.1006/meth.2001.1262. PubMed DOI
Krzyszczak A., Czech B. Occurrence and Toxicity of Polycyclic Aromatic Hydrocarbons Derivatives in Environmental Matrices. Sci. Total Environ. 2021;788:147738. doi: 10.1016/j.scitotenv.2021.147738. PubMed DOI
Keyte I.J., Albinet A., Harrison R.M. On-Road Traffic Emissions of Polycyclic Aromatic Hydrocarbons and Their Oxy- and Nitro- Derivative Compounds Measured in Road Tunnel Environments. Sci. Total Environ. 2016;566–567:1131–1142. doi: 10.1016/j.scitotenv.2016.05.152. PubMed DOI
Yang J., Roth P., Durbin T.D., Shafer M.M., Hemming J., Antkiewicz D.S., Asa-Awuku A., Karavalakis G. Emissions from a Flex Fuel GDI Vehicle Operating on Ethanol Fuels Show Marked Contrasts in Chemical, Physical and Toxicological Characteristics as a Function of Ethanol Content. Sci. Total Environ. 2019;683:749–761. doi: 10.1016/j.scitotenv.2019.05.279. PubMed DOI
Kostenidou E., Martinez-Valiente A., R’Mili B., Marques B., Temime-Roussel B., Durand A., André M., Liu Y., Louis C., Vansevenant B., et al. Technical Note: Emission Factors, Chemical Composition, and Morphology of Particles Emitted from Euro 5 Diesel and Gasoline Light-Duty Vehicles during Transient Cycles. Atmos. Chem. Phys. 2021;21:4779–4796. doi: 10.5194/acp-21-4779-2021. DOI
Pu X., Wang Z., Klaunig J.E. Alkaline Comet Assay for Assessing DNA Damage in Individual Cells. Curr. Protoc. Toxicol. 2015;65:3.12.1–3.12.11. doi: 10.1002/0471140856.tx0312s65. PubMed DOI
Shang Y., Zhou Q., Wang T., Jiang Y., Zhong Y., Qian G., Zhu T., Qiu X., An J. Airborne Nitro-PAHs Induce Nrf2/ARE Defense System against Oxidative Stress and Promote Inflammatory Process by Activating PI3K/Akt Pathway in A549 Cells. Toxicol. Vitr. 2017;44:66–73. doi: 10.1016/j.tiv.2017.06.017. PubMed DOI
Agarwal A.K., Singh A.P., Gupta T., Agarwal R.A., Sharma N., Pandey S.K., Ateeq B. Toxicity of Exhaust Particulates and Gaseous Emissions from Gasohol (Ethanol Blended Gasoline)-Fuelled Spark Ignition Engines. Environ. Sci. Process. Impacts. 2020;22:1540–1553. doi: 10.1039/D0EM00082E. PubMed DOI
Andrysík Z., Vondráček J., Marvanová S., Ciganek M., Neča J., Pěnčíková K., Mahadevan B., Topinka J., Baird W.M., Kozubík A., et al. Activation of the Aryl Hydrocarbon Receptor Is the Major Toxic Mode of Action of an Organic Extract of a Reference Urban Dust Particulate Matter Mixture: The Role of Polycyclic Aromatic Hydrocarbons. Mutat. Res.—Fundam. Mol. Mech. Mutagen. 2011;714:53–62. doi: 10.1016/j.mrfmmm.2011.06.011. PubMed DOI
Puga A., Ma C., Marlowe J.L. The Aryl Hydrocarbon Receptor Cross-Talks with Multiple Signal Transduction Pathways. Biochem. Pharmacol. 2009;77:713–722. doi: 10.1016/j.bcp.2008.08.031. PubMed DOI PMC
Líbalová H., Krčková S., Uhlířová K., Kléma J., Ciganek M., Rössner P., Šrám R.J., Vondráček J., Machala M., Topinka J. Analysis of Gene Expression Changes in A549 Cells Induced by Organic Compounds from Respirable Air Particles. Mutat. Res.—Fundam. Mol. Mech. Mutagen. 2014;770:94–105. doi: 10.1016/j.mrfmmm.2014.10.002. PubMed DOI
Vondráček J., Pěnčíková K., Ciganek M., Pivnička J., Karasová M., Hýžďalová M., Strapáčová S., Pálková L., Neča J., Matthews J., et al. Environmental Six-Ring Polycyclic Aromatic Hydrocarbons Are Potent Inducers of the AhR-Dependent Signaling in Human Cells. Environ. Pollut. 2020;266:115125. doi: 10.1016/j.envpol.2020.115125. PubMed DOI
Tauffenberger A., Magistretti P.J. Reactive Oxygen Species: Beyond Their Reactive Behavior. Neurochem. Res. 2021;46:77–87. doi: 10.1007/s11064-020-03208-7. PubMed DOI PMC
Black W., Chen Y., Matsumoto A., Thompson D.C., Lassen N., Pappa A., Vasiliou V. Molecular Mechanisms of ALDH3A1-Mediated Cellular Protection against 4-Hydroxy-2-Nonenal. Free Radic. Biol. Med. 2012;52:1937–1944. doi: 10.1016/j.freeradbiomed.2012.02.050. PubMed DOI PMC
Jang J.-H., Bruse S., Liu Y., Duffy V., Zhang C., Oyamada N., Randell S., Matsumoto A., Thompson D.C., Lin Y., et al. Aldehyde Dehydrogenase 3A1 Protects Airway Epithelial Cells from Cigarette Smoke-Induced DNA Damage and Cytotoxicity. Free Radic. Biol. Med. 2014;68:80–86. doi: 10.1016/j.freeradbiomed.2013.11.028. PubMed DOI PMC
Abbas I., Badran G., Verdin A., Ledoux F., Roumie M., Lo Guidice J.-M., Courcot D., Garçon G. In Vitro Evaluation of Organic Extractable Matter from Ambient PM(2.5) Using Human Bronchial Epithelial BEAS-2B Cells: Cytotoxicity, Oxidative Stress, pro-Inflammatory Response, Genotoxicity, and Cell Cycle Deregulation. Environ. Res. 2019;171:510–522. doi: 10.1016/j.envres.2019.01.052. PubMed DOI
Majoros H., Ujfaludi Z., Borsos B.N., Hudacsek V.V., Nagy Z., Coin F., Buzas K., Kovács I., Bíró T., Boros I.M., et al. SerpinB2 Is Involved in Cellular Response upon UV Irradiation. Sci. Rep. 2019;9:2753. doi: 10.1038/s41598-019-39073-w. PubMed DOI PMC
Hsieh H.-H., Chen Y.-C., Jhan J.-R., Lin J.-J. The Serine Protease Inhibitor SerpinB2 Binds and Stabilizes P21 in Senescent Cells. J. Cell Sci. 2017;130:3272–3281. doi: 10.1242/jcs.204974. PubMed DOI
Brauze D., Kiwerska K., Bednarek K., Grenman R., Janiszewska J., Giefing M., Jarmuz-Szymczak M. Expression of Serpin Peptidase Inhibitor B2 (SERPINB2) Is Regulated by Aryl Hydrocarbon Receptor (AhR) Chem. Biol. Interact. 2019;309:108700. doi: 10.1016/j.cbi.2019.06.013. PubMed DOI
Harris S.L., Levine A.J. The P53 Pathway: Positive and Negative Feedback Loops. Oncogene. 2005;24:2899–2908. doi: 10.1038/sj.onc.1208615. PubMed DOI
Vousden K.H., Lane D.P. P53 in Health and Disease. Nat. Rev. Mol. Cell Biol. 2007;8:275–283. doi: 10.1038/nrm2147. PubMed DOI
Skosareva L.V., Lebedeva N.A., Lavrik O.I., Rechkunova N.I. Repair of Bulky DNA Lesions Deriving from Polycyclic Aromatic Hydrocarbons. Mol. Biol. 2013;47:634–644. doi: 10.1134/S002689331305018X. PubMed DOI
Prado F. Homologous Recombination Maintenance of Genome Integrity during DNA Damage Tolerance. Mol. Cell. Oncol. 2014;1:e957039. doi: 10.4161/23723548.2014.957039. PubMed DOI PMC
Liu D., Xu Y. P53, Oxidative Stress, and Aging. Antioxid. Redox Signal. 2011;15:1669–1678. doi: 10.1089/ars.2010.3644. PubMed DOI PMC