Thinner inhalation effects on oxidative stress and DNA repair in a rat model of abuse

Humans can come into contact with thinner by occupational exposure or by intentional inhalation abuse. Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposu...

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Veröffentlicht in:Journal of applied toxicology 2010-04, Vol.30 (3), p.226-232
Hauptverfasser: Martínez-Alfaro, Minerva, Cárabez-Trejo, Alfonso, Gallegos-Corona, Marco-Antonio, Pedraza-Aboytes, Gustavo, Hernández-Chan, Nancy Georgina, Leo-Amador, Guillermo Enrique
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container_title Journal of applied toxicology
container_volume 30
creator Martínez-Alfaro, Minerva
Cárabez-Trejo, Alfonso
Gallegos-Corona, Marco-Antonio
Pedraza-Aboytes, Gustavo
Hernández-Chan, Nancy Georgina
Leo-Amador, Guillermo Enrique
description Humans can come into contact with thinner by occupational exposure or by intentional inhalation abuse. Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposure studies. In contrast, there is no data concerning the genotoxic effects of intentional inhalation abuse. The aim of this project was to examine the genotoxic effects of thinner inhalation in an animal model of thinner abuse (rats exposed to 3000 ppm toluene, a high solvent concentration over a very short, 15 min time period, twice a day for 6 weeks). The data presented here provides evidence that thinner inhalation in our experimental conditions is able to induce weight loss, lung abnormalities and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Lead treatment was used as a positive control in these assays. Finally, bone marrow was evaluated as a biomarker of cellular alteration associated with thinner inhalation. The observed absence of hemopoietic and genetic toxicity could be explained in part by the absence of benzene, the only carcinogenic component of thinner; however, benzene is no longer a common component of thinner. In conclusion, thinner did not cause genotoxic effects in an experimental model of intentional abuse despite the fact that thinner inhalation induces oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd. Genotoxic effects of thinner inhalation in an animal model of thinner abuse were examined. Thinner inhalation in our experimental condition is able to induce weight loss, lung abnormalities, and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Absence of hemopoietic and genotoxicity could be explained by the absence of benzene.
doi_str_mv 10.1002/jat.1488
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Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposure studies. In contrast, there is no data concerning the genotoxic effects of intentional inhalation abuse. The aim of this project was to examine the genotoxic effects of thinner inhalation in an animal model of thinner abuse (rats exposed to 3000 ppm toluene, a high solvent concentration over a very short, 15 min time period, twice a day for 6 weeks). The data presented here provides evidence that thinner inhalation in our experimental conditions is able to induce weight loss, lung abnormalities and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Lead treatment was used as a positive control in these assays. Finally, bone marrow was evaluated as a biomarker of cellular alteration associated with thinner inhalation. The observed absence of hemopoietic and genetic toxicity could be explained in part by the absence of benzene, the only carcinogenic component of thinner; however, benzene is no longer a common component of thinner. In conclusion, thinner did not cause genotoxic effects in an experimental model of intentional abuse despite the fact that thinner inhalation induces oxidative stress. Copyright © 2009 John Wiley &amp; Sons, Ltd. Genotoxic effects of thinner inhalation in an animal model of thinner abuse were examined. Thinner inhalation in our experimental condition is able to induce weight loss, lung abnormalities, and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Absence of hemopoietic and genotoxicity could be explained by the absence of benzene.</description><identifier>ISSN: 0260-437X</identifier><identifier>ISSN: 1099-1263</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.1488</identifier><identifier>PMID: 19885856</identifier><language>eng</language><publisher>Chichester, UK: John Wiley &amp; Sons, Ltd</publisher><subject>Animals ; Biomarkers - blood ; Biomarkers - metabolism ; Body Weight - drug effects ; Bone Marrow - drug effects ; Bone Marrow - pathology ; Disease Models, Animal ; DNA Damage - drug effects ; DNA Repair - drug effects ; Genotoxicity ; Inhalation Exposure - adverse effects ; Lung - drug effects ; Lung - metabolism ; Lung - pathology ; Lung Diseases - blood ; Lung Diseases - chemically induced ; Lung Diseases - metabolism ; Lung Diseases - pathology ; Lymphocytes - drug effects ; Lymphocytes - metabolism ; Male ; Malondialdehyde - blood ; Malondialdehyde - metabolism ; Mutagens - toxicity ; Oxidation-Reduction ; oxidative stress ; Oxidative Stress - drug effects ; Rats ; Rats, Sprague-Dawley ; Solvents - administration &amp; dosage ; Solvents - analysis ; Solvents - chemistry ; Solvents - toxicity ; Substance-Related Disorders - blood ; Substance-Related Disorders - metabolism ; Substance-Related Disorders - pathology ; Substance-Related Disorders - physiopathology ; thinner inhalation ; Time Factors ; Toluene - administration &amp; dosage ; Toluene - analysis ; Toluene - toxicity</subject><ispartof>Journal of applied toxicology, 2010-04, Vol.30 (3), p.226-232</ispartof><rights>Copyright © 2009 John Wiley &amp; Sons, Ltd.</rights><rights>(c) 2009 John Wiley &amp; Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4888-6e1e26f2d66aac14f609eccb991f7b572b86d89991585abd1d68dceaf1ff78c83</citedby><cites>FETCH-LOGICAL-c4888-6e1e26f2d66aac14f609eccb991f7b572b86d89991585abd1d68dceaf1ff78c83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjat.1488$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjat.1488$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19885856$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martínez-Alfaro, Minerva</creatorcontrib><creatorcontrib>Cárabez-Trejo, Alfonso</creatorcontrib><creatorcontrib>Gallegos-Corona, Marco-Antonio</creatorcontrib><creatorcontrib>Pedraza-Aboytes, Gustavo</creatorcontrib><creatorcontrib>Hernández-Chan, Nancy Georgina</creatorcontrib><creatorcontrib>Leo-Amador, Guillermo Enrique</creatorcontrib><title>Thinner inhalation effects on oxidative stress and DNA repair in a rat model of abuse</title><title>Journal of applied toxicology</title><addtitle>J. Appl. Toxicol</addtitle><description>Humans can come into contact with thinner by occupational exposure or by intentional inhalation abuse. Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposure studies. In contrast, there is no data concerning the genotoxic effects of intentional inhalation abuse. The aim of this project was to examine the genotoxic effects of thinner inhalation in an animal model of thinner abuse (rats exposed to 3000 ppm toluene, a high solvent concentration over a very short, 15 min time period, twice a day for 6 weeks). The data presented here provides evidence that thinner inhalation in our experimental conditions is able to induce weight loss, lung abnormalities and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Lead treatment was used as a positive control in these assays. Finally, bone marrow was evaluated as a biomarker of cellular alteration associated with thinner inhalation. The observed absence of hemopoietic and genetic toxicity could be explained in part by the absence of benzene, the only carcinogenic component of thinner; however, benzene is no longer a common component of thinner. In conclusion, thinner did not cause genotoxic effects in an experimental model of intentional abuse despite the fact that thinner inhalation induces oxidative stress. Copyright © 2009 John Wiley &amp; Sons, Ltd. Genotoxic effects of thinner inhalation in an animal model of thinner abuse were examined. Thinner inhalation in our experimental condition is able to induce weight loss, lung abnormalities, and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. 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dosage</subject><subject>Solvents - analysis</subject><subject>Solvents - chemistry</subject><subject>Solvents - toxicity</subject><subject>Substance-Related Disorders - blood</subject><subject>Substance-Related Disorders - metabolism</subject><subject>Substance-Related Disorders - pathology</subject><subject>Substance-Related Disorders - physiopathology</subject><subject>thinner inhalation</subject><subject>Time Factors</subject><subject>Toluene - administration &amp; dosage</subject><subject>Toluene - analysis</subject><subject>Toluene - toxicity</subject><issn>0260-437X</issn><issn>1099-1263</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOAyEUhonRaL0kPoFhp5tRYDoMLBsvVaN1U6NxQxg4RHQ6U2Hq5e2l6URXxhUH-M5_Tj6E9ik5poSwkxfdHdOhEGtoQImUGWU8X0cDwjjJhnn5uIW2Y3whJP0xsYm2qBSiEAUfoPvps28aCNg3z7rWnW8bDM6B6SJOZfvpbXp8Bxy7ADFi3Vh8NhnhAHPtl11Y46A7PGst1Lh1WFeLCLtow-k6wl5_7qD7i_Pp6WV2cze-Oh3dZCYtKzIOFBh3zHKutaFDx4kEYyopqSuromSV4FbIdE3L6spSy4U1oB11rhRG5DvocJU7D-3bAmKnZj4aqGvdQLuISoh86YAW_5Ncphk5k4k8WpEmtDEGcGoe_EyHL0WJWtpWybZa2k7oQR-6qGZgf8FebwKyFfDha_j6M0hdj6Z9YM_72MHnD6_Dq-JlXhbqYTJWt4w-TMpyrJ7yb-mDl7M</recordid><startdate>201004</startdate><enddate>201004</enddate><creator>Martínez-Alfaro, Minerva</creator><creator>Cárabez-Trejo, Alfonso</creator><creator>Gallegos-Corona, Marco-Antonio</creator><creator>Pedraza-Aboytes, Gustavo</creator><creator>Hernández-Chan, Nancy Georgina</creator><creator>Leo-Amador, Guillermo Enrique</creator><general>John Wiley &amp; 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Appl. Toxicol</addtitle><date>2010-04</date><risdate>2010</risdate><volume>30</volume><issue>3</issue><spage>226</spage><epage>232</epage><pages>226-232</pages><issn>0260-437X</issn><issn>1099-1263</issn><eissn>1099-1263</eissn><abstract>Humans can come into contact with thinner by occupational exposure or by intentional inhalation abuse. Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposure studies. In contrast, there is no data concerning the genotoxic effects of intentional inhalation abuse. The aim of this project was to examine the genotoxic effects of thinner inhalation in an animal model of thinner abuse (rats exposed to 3000 ppm toluene, a high solvent concentration over a very short, 15 min time period, twice a day for 6 weeks). The data presented here provides evidence that thinner inhalation in our experimental conditions is able to induce weight loss, lung abnormalities and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Lead treatment was used as a positive control in these assays. Finally, bone marrow was evaluated as a biomarker of cellular alteration associated with thinner inhalation. The observed absence of hemopoietic and genetic toxicity could be explained in part by the absence of benzene, the only carcinogenic component of thinner; however, benzene is no longer a common component of thinner. In conclusion, thinner did not cause genotoxic effects in an experimental model of intentional abuse despite the fact that thinner inhalation induces oxidative stress. Copyright © 2009 John Wiley &amp; Sons, Ltd. Genotoxic effects of thinner inhalation in an animal model of thinner abuse were examined. Thinner inhalation in our experimental condition is able to induce weight loss, lung abnormalities, and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Absence of hemopoietic and genotoxicity could be explained by the absence of benzene.</abstract><cop>Chichester, UK</cop><pub>John Wiley &amp; Sons, Ltd</pub><pmid>19885856</pmid><doi>10.1002/jat.1488</doi><tpages>7</tpages></addata></record>
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subjects Animals
Biomarkers - blood
Biomarkers - metabolism
Body Weight - drug effects
Bone Marrow - drug effects
Bone Marrow - pathology
Disease Models, Animal
DNA Damage - drug effects
DNA Repair - drug effects
Genotoxicity
Inhalation Exposure - adverse effects
Lung - drug effects
Lung - metabolism
Lung - pathology
Lung Diseases - blood
Lung Diseases - chemically induced
Lung Diseases - metabolism
Lung Diseases - pathology
Lymphocytes - drug effects
Lymphocytes - metabolism
Male
Malondialdehyde - blood
Malondialdehyde - metabolism
Mutagens - toxicity
Oxidation-Reduction
oxidative stress
Oxidative Stress - drug effects
Rats
Rats, Sprague-Dawley
Solvents - administration & dosage
Solvents - analysis
Solvents - chemistry
Solvents - toxicity
Substance-Related Disorders - blood
Substance-Related Disorders - metabolism
Substance-Related Disorders - pathology
Substance-Related Disorders - physiopathology
thinner inhalation
Time Factors
Toluene - administration & dosage
Toluene - analysis
Toluene - toxicity
title Thinner inhalation effects on oxidative stress and DNA repair in a rat model of abuse
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