Carcinogenicity of acrolein, crotonaldehyde, and arecoline
Acrolein alters cell proliferation, cell death, or nutrient supply, inhibiting tumour suppressor genes and activating proto-oncogenes in cultured human and rodent cells, and inducing hyperplasia and metaplasia in the rodent respiratory system.2,3 Overall, there is “strong” evidence that acrolein exh...
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creator | Marques, M Matilde Beland, Frederick A Lachenmeier, Dirk W Phillips, David H Chung, Fung-Lung Dorman, David C Elmore, Sarah E Hammond, S Katharine Krstev, Srmena Linhart, Igor Long, Alexandra S Mandrioli, Daniele Ogawa, Kumiko Pappas, Jane J Parra Morte, Juan M Talaska, Glenn Tang, Moon-shong Thakur, Nisha van Tongeren, Martie Vineis, Paolo Grosse, Yann Benbrahim-Tallaa, Lamia Suonio, Eero Turner, Michelle C El Ghissassi, Fatiha Middleton, Daniel Miranda-Filho, Adalberto Chung, Felicia Liu, Yaqi Vega, Samantha Mattock, Heidi Schubauer-Berigan, Mary K Guyton, Kathryn Z |
description | Acrolein alters cell proliferation, cell death, or nutrient supply, inhibiting tumour suppressor genes and activating proto-oncogenes in cultured human and rodent cells, and inducing hyperplasia and metaplasia in the rodent respiratory system.2,3 Overall, there is “strong” evidence that acrolein exhibits multiple key characteristics of carcinogens, primarily from studies with human primary cells and studies in experimental systems, supported by studies in humans on DNA adducts. An electrophilic α,β-unsaturated aldehyde (enal), crotonaldehyde forms cyclic adducts in DNA as well as DNA interstrand and DNA–protein cross-links. α-Methyl-γ-hydroxy-1,N2-propanodeoxyguanosine has been detected in human saliva, urine, blood, mammary tissue, oral (gingival) tissue, liver, and placenta.4,5 Adduct levels were significantly elevated in tobacco smokers.4 Crotonaldehyde-derived DNA adducts have also been detected in human cells in vitro and in rodents. Crotonaldehyde is genotoxic, exhibiting clastogenicity in human primary cells and human cell lines,8 dominant lethality and chromosomal aberrations in rodents, and gene mutations in cultured rodent cells, Drosophila melanogaster, Salmonella typhimurium, and plasmid systems. |
doi_str_mv | 10.1016/S1470-2045(20)30727-0 |
format | Article |
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An electrophilic α,β-unsaturated aldehyde (enal), crotonaldehyde forms cyclic adducts in DNA as well as DNA interstrand and DNA–protein cross-links. α-Methyl-γ-hydroxy-1,N2-propanodeoxyguanosine has been detected in human saliva, urine, blood, mammary tissue, oral (gingival) tissue, liver, and placenta.4,5 Adduct levels were significantly elevated in tobacco smokers.4 Crotonaldehyde-derived DNA adducts have also been detected in human cells in vitro and in rodents. Crotonaldehyde is genotoxic, exhibiting clastogenicity in human primary cells and human cell lines,8 dominant lethality and chromosomal aberrations in rodents, and gene mutations in cultured rodent cells, Drosophila melanogaster, Salmonella typhimurium, and plasmid systems.</description><identifier>ISSN: 1470-2045</identifier><identifier>EISSN: 1474-5488</identifier><identifier>DOI: 10.1016/S1470-2045(20)30727-0</identifier><identifier>PMID: 33248467</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Acrolein ; Acrolein - toxicity ; Air pollution ; Aldehydes - toxicity ; Animals ; Arecoline - toxicity ; Cancer ; Carcinogenicity ; Carcinogenicity Tests ; Carcinogens ; Carcinogens, Environmental - toxicity ; Cell death ; Cell proliferation ; Chromosome aberrations ; Clastogenicity ; Consensus Development Conferences as Topic ; Deoxyribonucleic acid ; DNA ; DNA adducts ; Electronic cigarettes ; Environmental Exposure - adverse effects ; Genotoxicity ; Humans ; Hyperplasia ; Internet ; Lethality ; Metaplasia ; Mutation ; Neoplasms - chemically induced ; Oxidative stress ; Placenta ; Proteins ; Proto-oncogenes ; Respiratory system ; Risk Assessment ; Rodents ; Saliva ; Telecommunications ; Tobacco ; Tumor suppressor genes ; Tumors ; Urine</subject><ispartof>The lancet oncology, 2021-01, Vol.22 (1), p.19-20</ispartof><rights>2021 Elsevier Ltd</rights><rights>2021. Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-d2bb4c48958c1cb1e06e834eb997cd86ae7bc4582bb16344c574740be5627fdc3</citedby><cites>FETCH-LOGICAL-c445t-d2bb4c48958c1cb1e06e834eb997cd86ae7bc4582bb16344c574740be5627fdc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1470204520307270$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33248467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marques, M Matilde</creatorcontrib><creatorcontrib>Beland, Frederick A</creatorcontrib><creatorcontrib>Lachenmeier, Dirk W</creatorcontrib><creatorcontrib>Phillips, David H</creatorcontrib><creatorcontrib>Chung, Fung-Lung</creatorcontrib><creatorcontrib>Dorman, David C</creatorcontrib><creatorcontrib>Elmore, Sarah E</creatorcontrib><creatorcontrib>Hammond, S Katharine</creatorcontrib><creatorcontrib>Krstev, Srmena</creatorcontrib><creatorcontrib>Linhart, Igor</creatorcontrib><creatorcontrib>Long, Alexandra S</creatorcontrib><creatorcontrib>Mandrioli, Daniele</creatorcontrib><creatorcontrib>Ogawa, Kumiko</creatorcontrib><creatorcontrib>Pappas, Jane J</creatorcontrib><creatorcontrib>Parra Morte, Juan M</creatorcontrib><creatorcontrib>Talaska, Glenn</creatorcontrib><creatorcontrib>Tang, Moon-shong</creatorcontrib><creatorcontrib>Thakur, Nisha</creatorcontrib><creatorcontrib>van Tongeren, Martie</creatorcontrib><creatorcontrib>Vineis, Paolo</creatorcontrib><creatorcontrib>Grosse, Yann</creatorcontrib><creatorcontrib>Benbrahim-Tallaa, Lamia</creatorcontrib><creatorcontrib>Suonio, Eero</creatorcontrib><creatorcontrib>Turner, Michelle C</creatorcontrib><creatorcontrib>El Ghissassi, Fatiha</creatorcontrib><creatorcontrib>Middleton, Daniel</creatorcontrib><creatorcontrib>Miranda-Filho, Adalberto</creatorcontrib><creatorcontrib>Chung, Felicia</creatorcontrib><creatorcontrib>Liu, Yaqi</creatorcontrib><creatorcontrib>Vega, Samantha</creatorcontrib><creatorcontrib>Mattock, Heidi</creatorcontrib><creatorcontrib>Schubauer-Berigan, Mary K</creatorcontrib><creatorcontrib>Guyton, Kathryn Z</creatorcontrib><creatorcontrib>IARC Monographs Vol 128 group</creatorcontrib><title>Carcinogenicity of acrolein, crotonaldehyde, and arecoline</title><title>The lancet oncology</title><addtitle>Lancet Oncol</addtitle><description>Acrolein alters cell proliferation, cell death, or nutrient supply, inhibiting tumour suppressor genes and activating proto-oncogenes in cultured human and rodent cells, and inducing hyperplasia and metaplasia in the rodent respiratory system.2,3 Overall, there is “strong” evidence that acrolein exhibits multiple key characteristics of carcinogens, primarily from studies with human primary cells and studies in experimental systems, supported by studies in humans on DNA adducts. An electrophilic α,β-unsaturated aldehyde (enal), crotonaldehyde forms cyclic adducts in DNA as well as DNA interstrand and DNA–protein cross-links. α-Methyl-γ-hydroxy-1,N2-propanodeoxyguanosine has been detected in human saliva, urine, blood, mammary tissue, oral (gingival) tissue, liver, and placenta.4,5 Adduct levels were significantly elevated in tobacco smokers.4 Crotonaldehyde-derived DNA adducts have also been detected in human cells in vitro and in rodents. Crotonaldehyde is genotoxic, exhibiting clastogenicity in human primary cells and human cell lines,8 dominant lethality and chromosomal aberrations in rodents, and gene mutations in cultured rodent cells, Drosophila melanogaster, Salmonella typhimurium, and plasmid systems.</description><subject>Acrolein</subject><subject>Acrolein - toxicity</subject><subject>Air pollution</subject><subject>Aldehydes - toxicity</subject><subject>Animals</subject><subject>Arecoline - toxicity</subject><subject>Cancer</subject><subject>Carcinogenicity</subject><subject>Carcinogenicity Tests</subject><subject>Carcinogens</subject><subject>Carcinogens, Environmental - toxicity</subject><subject>Cell death</subject><subject>Cell proliferation</subject><subject>Chromosome aberrations</subject><subject>Clastogenicity</subject><subject>Consensus Development Conferences as Topic</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA adducts</subject><subject>Electronic cigarettes</subject><subject>Environmental Exposure - adverse effects</subject><subject>Genotoxicity</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Internet</subject><subject>Lethality</subject><subject>Metaplasia</subject><subject>Mutation</subject><subject>Neoplasms - chemically induced</subject><subject>Oxidative stress</subject><subject>Placenta</subject><subject>Proteins</subject><subject>Proto-oncogenes</subject><subject>Respiratory system</subject><subject>Risk Assessment</subject><subject>Rodents</subject><subject>Saliva</subject><subject>Telecommunications</subject><subject>Tobacco</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><subject>Urine</subject><issn>1470-2045</issn><issn>1474-5488</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkE1LAzEQQIMotlZ_grLgRaGrSTbZpF5Eil9Q8KCeQzaZ1ZTtpiZbof_etFu9epkZwpvJzEPolOArgkl5_UqYwDnFjF9QfFlgQUWO99AwPbOcMyn3t3WPDNBRjHOMiSCYH6JBUVAmWSmG6Gaqg3Gt_4DWGdetM19n2gTfgGvHWSo63-rGwufawjjTrc10AOMb18IxOqh1E-Fkl0fo_eH-bfqUz14en6d3s9wwxrvc0qpihskJl4aYigAuQRYMqslEGCtLDaIyjMuEkbJgzHCRTsAV8JKK2ppihM77ucvgv1YQOzX3q5C2ioomkoiCEpIo3lNp5xgD1GoZ3EKHtSJYbYyprTG10ZGC2hpTOPWd7aavqgXYv65fRQm47QFIN347CCoaB60B65KJTlnv_vniB8SXeao</recordid><startdate>202101</startdate><enddate>202101</enddate><creator>Marques, M Matilde</creator><creator>Beland, Frederick A</creator><creator>Lachenmeier, Dirk W</creator><creator>Phillips, David H</creator><creator>Chung, Fung-Lung</creator><creator>Dorman, David C</creator><creator>Elmore, 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Katharine ; Krstev, Srmena ; Linhart, Igor ; Long, Alexandra S ; Mandrioli, Daniele ; Ogawa, Kumiko ; Pappas, Jane J ; Parra Morte, Juan M ; Talaska, Glenn ; Tang, Moon-shong ; Thakur, Nisha ; van Tongeren, Martie ; Vineis, Paolo ; Grosse, Yann ; Benbrahim-Tallaa, Lamia ; Suonio, Eero ; Turner, Michelle C ; El Ghissassi, Fatiha ; Middleton, Daniel ; Miranda-Filho, Adalberto ; Chung, Felicia ; Liu, Yaqi ; Vega, Samantha ; Mattock, Heidi ; Schubauer-Berigan, Mary K ; Guyton, Kathryn Z</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-d2bb4c48958c1cb1e06e834eb997cd86ae7bc4582bb16344c574740be5627fdc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acrolein</topic><topic>Acrolein - toxicity</topic><topic>Air pollution</topic><topic>Aldehydes - toxicity</topic><topic>Animals</topic><topic>Arecoline - 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An electrophilic α,β-unsaturated aldehyde (enal), crotonaldehyde forms cyclic adducts in DNA as well as DNA interstrand and DNA–protein cross-links. α-Methyl-γ-hydroxy-1,N2-propanodeoxyguanosine has been detected in human saliva, urine, blood, mammary tissue, oral (gingival) tissue, liver, and placenta.4,5 Adduct levels were significantly elevated in tobacco smokers.4 Crotonaldehyde-derived DNA adducts have also been detected in human cells in vitro and in rodents. Crotonaldehyde is genotoxic, exhibiting clastogenicity in human primary cells and human cell lines,8 dominant lethality and chromosomal aberrations in rodents, and gene mutations in cultured rodent cells, Drosophila melanogaster, Salmonella typhimurium, and plasmid systems.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>33248467</pmid><doi>10.1016/S1470-2045(20)30727-0</doi><tpages>2</tpages></addata></record> |
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source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | Acrolein Acrolein - toxicity Air pollution Aldehydes - toxicity Animals Arecoline - toxicity Cancer Carcinogenicity Carcinogenicity Tests Carcinogens Carcinogens, Environmental - toxicity Cell death Cell proliferation Chromosome aberrations Clastogenicity Consensus Development Conferences as Topic Deoxyribonucleic acid DNA DNA adducts Electronic cigarettes Environmental Exposure - adverse effects Genotoxicity Humans Hyperplasia Internet Lethality Metaplasia Mutation Neoplasms - chemically induced Oxidative stress Placenta Proteins Proto-oncogenes Respiratory system Risk Assessment Rodents Saliva Telecommunications Tobacco Tumor suppressor genes Tumors Urine |
title | Carcinogenicity of acrolein, crotonaldehyde, and arecoline |
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