Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray
Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced in the combustion of organic matter. Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogen...
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| Veröffentlicht in: | Environmental toxicology 2013-11, Vol.28 (11), p.652-659 |
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| description | Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced in the combustion of organic matter. Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogenomics in the recent years. To evaluate the mutagenicity of PAHs and constituents of environmental pollutants in lung tissue, including metabolic activation, human alveolar epithelial type II cells (A549) were treated with nonmutagenic PAH pyrene and with the mutagenic PAHs benzo‐[a]‐pyrene, 1‐nitropyrene, or 1,8‐dinitropyrene. Comparison of genome‐wide microarray expression profiles between a nonmutagenic and a mutagenic PAH‐treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53‐downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH‐treated group. Pretreatment with cytochrome P450 inhibitor α‐naphthoflavone or p53 inhibitor pifithrin‐α inhibited the benzo‐[a]‐pyrene‐induced p21 expression. These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages‐recognition signal is converged with p53 downstream genes. This metabolic activation and DNA damage is induced in lung epithelium, and the mutagenicity of PAHs can be classified by DNA microarray expression profiles. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28:652–659, 2013. |
| doi_str_mv | 10.1002/tox.20761 |
| format | Article |
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Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogenomics in the recent years. To evaluate the mutagenicity of PAHs and constituents of environmental pollutants in lung tissue, including metabolic activation, human alveolar epithelial type II cells (A549) were treated with nonmutagenic PAH pyrene and with the mutagenic PAHs benzo‐[a]‐pyrene, 1‐nitropyrene, or 1,8‐dinitropyrene. Comparison of genome‐wide microarray expression profiles between a nonmutagenic and a mutagenic PAH‐treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53‐downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH‐treated group. Pretreatment with cytochrome P450 inhibitor α‐naphthoflavone or p53 inhibitor pifithrin‐α inhibited the benzo‐[a]‐pyrene‐induced p21 expression. These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages‐recognition signal is converged with p53 downstream genes. This metabolic activation and DNA damage is induced in lung epithelium, and the mutagenicity of PAHs can be classified by DNA microarray expression profiles. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28:652–659, 2013.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.20761</identifier><identifier>PMID: 21887816</identifier><identifier>CODEN: ETOXFH</identifier><language>eng</language><publisher>Hoboken, NJ: Blackwell Publishing Ltd</publisher><subject>Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors ; Aryl Hydrocarbon Hydroxylases - genetics ; Benzoflavones - pharmacology ; Benzothiazoles - pharmacology ; Biological and medical sciences ; cancer ; Cell Line ; cytochrome P450 ; DNA Damage ; DNA microarray ; Environmental Pollutants - classification ; Environmental Pollutants - toxicity ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Ontology ; General aspects. Methods ; Genes, p53 ; Humans ; lung ; Lung - cytology ; Lung - drug effects ; Lung - metabolism ; Medical sciences ; metabolic activation ; mutagenicity ; Mutagenicity Tests ; Oligonucleotide Array Sequence Analysis ; p53 ; PAH ; polycyclic aromatic hydrocarbon ; Polycyclic Aromatic Hydrocarbons - classification ; Polycyclic Aromatic Hydrocarbons - toxicity ; Pulmonary Alveoli - cytology ; Pulmonary Alveoli - drug effects ; Pulmonary Alveoli - metabolism ; Respiratory Mucosa - cytology ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - metabolism ; Toluene - analogs & derivatives ; Toluene - pharmacology ; Toxicology</subject><ispartof>Environmental toxicology, 2013-11, Vol.28 (11), p.652-659</ispartof><rights>Copyright © 2011 Wiley Periodicals, Inc., A Wiley Company</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Wiley Periodicals, Inc., A Wiley Company.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4201-fbd42a96ffdfc470bcfcf4cb1da4f7429d638ef732a6f621c4a07a0446d88f433</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.20761$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.20761$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27994737$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21887816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirano, Minoru</creatorcontrib><creatorcontrib>Tanaka, Shiho</creatorcontrib><creatorcontrib>Asami, Osamu</creatorcontrib><title>Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray</title><title>Environmental toxicology</title><addtitle>Environ. Toxicol</addtitle><description>Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced in the combustion of organic matter. Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogenomics in the recent years. To evaluate the mutagenicity of PAHs and constituents of environmental pollutants in lung tissue, including metabolic activation, human alveolar epithelial type II cells (A549) were treated with nonmutagenic PAH pyrene and with the mutagenic PAHs benzo‐[a]‐pyrene, 1‐nitropyrene, or 1,8‐dinitropyrene. Comparison of genome‐wide microarray expression profiles between a nonmutagenic and a mutagenic PAH‐treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53‐downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH‐treated group. Pretreatment with cytochrome P450 inhibitor α‐naphthoflavone or p53 inhibitor pifithrin‐α inhibited the benzo‐[a]‐pyrene‐induced p21 expression. These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages‐recognition signal is converged with p53 downstream genes. This metabolic activation and DNA damage is induced in lung epithelium, and the mutagenicity of PAHs can be classified by DNA microarray expression profiles. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28:652–659, 2013.</description><subject>Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors</subject><subject>Aryl Hydrocarbon Hydroxylases - genetics</subject><subject>Benzoflavones - pharmacology</subject><subject>Benzothiazoles - pharmacology</subject><subject>Biological and medical sciences</subject><subject>cancer</subject><subject>Cell Line</subject><subject>cytochrome P450</subject><subject>DNA Damage</subject><subject>DNA microarray</subject><subject>Environmental Pollutants - classification</subject><subject>Environmental Pollutants - toxicity</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Gene Ontology</subject><subject>General aspects. Methods</subject><subject>Genes, p53</subject><subject>Humans</subject><subject>lung</subject><subject>Lung - cytology</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Medical sciences</subject><subject>metabolic activation</subject><subject>mutagenicity</subject><subject>Mutagenicity Tests</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>p53</subject><subject>PAH</subject><subject>polycyclic aromatic hydrocarbon</subject><subject>Polycyclic Aromatic Hydrocarbons - classification</subject><subject>Polycyclic Aromatic Hydrocarbons - toxicity</subject><subject>Pulmonary Alveoli - cytology</subject><subject>Pulmonary Alveoli - drug effects</subject><subject>Pulmonary Alveoli - metabolism</subject><subject>Respiratory Mucosa - cytology</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Toluene - analogs & derivatives</subject><subject>Toluene - pharmacology</subject><subject>Toxicology</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0U1v3CAQBmCratV8tIf-gQqpipSLE8AY8DHatptWUXJJldzQGMMuqQ1bsJX435fubhMpJ0bwzGjEWxSfCD4jGNPzMTydUSw4eVMckprSUlAh325rXDIsyUFxlNIDxrjhNX9fHFAipZCEHxZ-0UNKzjoNowseBYs2oZ_1rHunEcQw5HuN1nMXg4bYBp9QC8l0KONhGmFlvNNunJHzqJ_8Co0upcmgcR3DtFqjr9cXaHA6BogR5g_FOwt9Mh_353Hx6_u328VleXWz_LG4uCo1o5iUtu0YhYZb21nNBG611ZbplnTArGC06XgljRUVBW45JZoBFoAZ452UllXVcXG6m7uJ4c9k0qgGl7Tpe_AmTEkRxmXFMKtlpl9e0YcwRZ-3y4pVXEhZN1l93qupHUynNtENEGf1_yczONkDSBp6G8Frl16caBomKpHd-c49ut7Mz-8Eq39Rqhyl2kapbm_ut0XuKHcdLo3m6bkD4m_F88Ra3V0vlby7xD-XC6Luq7_Z2KEF</recordid><startdate>201311</startdate><enddate>201311</enddate><creator>Hirano, Minoru</creator><creator>Tanaka, Shiho</creator><creator>Asami, Osamu</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7T2</scope><scope>7TM</scope><scope>7TV</scope><scope>7U1</scope><scope>7U2</scope></search><sort><creationdate>201311</creationdate><title>Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray</title><author>Hirano, Minoru ; Tanaka, Shiho ; Asami, Osamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4201-fbd42a96ffdfc470bcfcf4cb1da4f7429d638ef732a6f621c4a07a0446d88f433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors</topic><topic>Aryl Hydrocarbon Hydroxylases - genetics</topic><topic>Benzoflavones - pharmacology</topic><topic>Benzothiazoles - pharmacology</topic><topic>Biological and medical sciences</topic><topic>cancer</topic><topic>Cell Line</topic><topic>cytochrome P450</topic><topic>DNA Damage</topic><topic>DNA microarray</topic><topic>Environmental Pollutants - classification</topic><topic>Environmental Pollutants - toxicity</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Gene Ontology</topic><topic>General aspects. Methods</topic><topic>Genes, p53</topic><topic>Humans</topic><topic>lung</topic><topic>Lung - cytology</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Medical sciences</topic><topic>metabolic activation</topic><topic>mutagenicity</topic><topic>Mutagenicity Tests</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>p53</topic><topic>PAH</topic><topic>polycyclic aromatic hydrocarbon</topic><topic>Polycyclic Aromatic Hydrocarbons - classification</topic><topic>Polycyclic Aromatic Hydrocarbons - toxicity</topic><topic>Pulmonary Alveoli - cytology</topic><topic>Pulmonary Alveoli - drug effects</topic><topic>Pulmonary Alveoli - metabolism</topic><topic>Respiratory Mucosa - cytology</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Toluene - analogs & derivatives</topic><topic>Toluene - pharmacology</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirano, Minoru</creatorcontrib><creatorcontrib>Tanaka, Shiho</creatorcontrib><creatorcontrib>Asami, Osamu</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Nucleic Acids Abstracts</collection><collection>Pollution Abstracts</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirano, Minoru</au><au>Tanaka, Shiho</au><au>Asami, Osamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ. Toxicol</addtitle><date>2013-11</date><risdate>2013</risdate><volume>28</volume><issue>11</issue><spage>652</spage><epage>659</epage><pages>652-659</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><coden>ETOXFH</coden><abstract>Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced in the combustion of organic matter. Exposure to PAHs raises the risk of lung cancer and inflammatory and allergic disorders such as asthma. DNA microarray technologies have been applied to research on toxicogenomics in the recent years. To evaluate the mutagenicity of PAHs and constituents of environmental pollutants in lung tissue, including metabolic activation, human alveolar epithelial type II cells (A549) were treated with nonmutagenic PAH pyrene and with the mutagenic PAHs benzo‐[a]‐pyrene, 1‐nitropyrene, or 1,8‐dinitropyrene. Comparison of genome‐wide microarray expression profiles between a nonmutagenic and a mutagenic PAH‐treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53‐downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH‐treated group. Pretreatment with cytochrome P450 inhibitor α‐naphthoflavone or p53 inhibitor pifithrin‐α inhibited the benzo‐[a]‐pyrene‐induced p21 expression. These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages‐recognition signal is converged with p53 downstream genes. This metabolic activation and DNA damage is induced in lung epithelium, and the mutagenicity of PAHs can be classified by DNA microarray expression profiles. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28:652–659, 2013.</abstract><cop>Hoboken, NJ</cop><pub>Blackwell Publishing Ltd</pub><pmid>21887816</pmid><doi>10.1002/tox.20761</doi><tpages>8</tpages></addata></record> |
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| subjects | Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors Aryl Hydrocarbon Hydroxylases - genetics Benzoflavones - pharmacology Benzothiazoles - pharmacology Biological and medical sciences cancer Cell Line cytochrome P450 DNA Damage DNA microarray Environmental Pollutants - classification Environmental Pollutants - toxicity Gene Expression Profiling Gene Expression Regulation Gene Ontology General aspects. Methods Genes, p53 Humans lung Lung - cytology Lung - drug effects Lung - metabolism Medical sciences metabolic activation mutagenicity Mutagenicity Tests Oligonucleotide Array Sequence Analysis p53 PAH polycyclic aromatic hydrocarbon Polycyclic Aromatic Hydrocarbons - classification Polycyclic Aromatic Hydrocarbons - toxicity Pulmonary Alveoli - cytology Pulmonary Alveoli - drug effects Pulmonary Alveoli - metabolism Respiratory Mucosa - cytology Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Toluene - analogs & derivatives Toluene - pharmacology Toxicology |
| title | Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray |
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