Genomic and transcriptional alterations in mouse fetus liver after transplacental exposure to cigarette smoke
ABSTRACT The transplacental exposure of fetuses to maternal cigarette smoke may increase the risk of developmental impairments, congenital diseases, and childhood cancer. The whole‐body exposure of Swiss mice to environmental cigarette smoke (ECS) during pregnancy decreased the number of fetuses per...
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| creator | Izzotti, Alberto Balansky, Roumen M. Cartiglia, Cristina Camoirano, Anna Longobardi, Mariagrazia De Flora, Silvio |
| description | ABSTRACT
The transplacental exposure of fetuses to maternal cigarette smoke may increase the risk of developmental impairments, congenital diseases, and childhood cancer. The whole‐body exposure of Swiss mice to environmental cigarette smoke (ECS) during pregnancy decreased the number of fetuses per dam, placenta weight, and fetus weight. ECS increased DNA adducts, oxidative nucleotide alterations, and cytogenetic damage in fetus liver. Evaluation by cDNA array of 746 genes showed that 61 of them were expressed in fetus liver under basal conditions. The oral administration of N‐acetylcysteine (NAC) during pregnancy enhanced the expression of three genes only, including two glutathione S‐transferases and α1‐antitrypsin precursor, whose deficiency plays a pathogenetic role in congenital emphysema. Transplacental ECS upregulated the expression of 116 genes involved in metabolism, response to oxidative stress, DNA and protein repair, and signal transduction. NAC inhibited the ECS‐related genetic damage and upregulation of most genes. ECS stimulated pro‐apoptotic genes and genes downregulating the cell cycle, which may justify growth impairments in the developing fetus. Thus, both genetic and epigenetic mechanisms were modulated by ECS. Moreover, hypoxia‐related genes and several oncogenes and receptors involved in proliferation and differentiation of leukocytes were induced in the fetal liver, which also bears hematopoietic functions. |
| doi_str_mv | 10.1096/fj.02-0967fje |
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The transplacental exposure of fetuses to maternal cigarette smoke may increase the risk of developmental impairments, congenital diseases, and childhood cancer. The whole‐body exposure of Swiss mice to environmental cigarette smoke (ECS) during pregnancy decreased the number of fetuses per dam, placenta weight, and fetus weight. ECS increased DNA adducts, oxidative nucleotide alterations, and cytogenetic damage in fetus liver. Evaluation by cDNA array of 746 genes showed that 61 of them were expressed in fetus liver under basal conditions. The oral administration of N‐acetylcysteine (NAC) during pregnancy enhanced the expression of three genes only, including two glutathione S‐transferases and α1‐antitrypsin precursor, whose deficiency plays a pathogenetic role in congenital emphysema. Transplacental ECS upregulated the expression of 116 genes involved in metabolism, response to oxidative stress, DNA and protein repair, and signal transduction. NAC inhibited the ECS‐related genetic damage and upregulation of most genes. ECS stimulated pro‐apoptotic genes and genes downregulating the cell cycle, which may justify growth impairments in the developing fetus. Thus, both genetic and epigenetic mechanisms were modulated by ECS. Moreover, hypoxia‐related genes and several oncogenes and receptors involved in proliferation and differentiation of leukocytes were induced in the fetal liver, which also bears hematopoietic functions.</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.02-0967fje</identifier><identifier>PMID: 12709406</identifier><language>eng</language><publisher>United States: Federation of American Societies for Experimental Biology</publisher><subject>Acetylcysteine - pharmacology ; Animals ; Anticarcinogenic Agents - pharmacology ; Apoptosis ; Cell Cycle - drug effects ; Cell Division - drug effects ; Cell Hypoxia ; DNA Adducts - metabolism ; DNA Repair ; Female ; Fetus - anatomy & histology ; Fetus - drug effects ; Gene Expression Regulation - drug effects ; Genome ; genomic alterations ; Hematopoietic Stem Cells - cytology ; Hematopoietic Stem Cells - drug effects ; Liver - drug effects ; Liver - embryology ; Liver - metabolism ; Maternal Exposure ; Mice ; mouse liver development ; multigene expression analysis ; N‐acetylcysteine ; Oxidation-Reduction ; Oxidative Stress ; Parity - drug effects ; Placenta - anatomy & histology ; Placenta - drug effects ; Pregnancy ; Smoking - adverse effects ; Transcription, Genetic ; transplacental cigarette smoke</subject><ispartof>The FASEB journal, 2003-06, Vol.17 (9), p.1127-1129</ispartof><rights>FASEB</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371E-2a2decca88475f07b54b73c4c21e8f60cddde5bfccc9496ef7b8c120915114a53</citedby><cites>FETCH-LOGICAL-c371E-2a2decca88475f07b54b73c4c21e8f60cddde5bfccc9496ef7b8c120915114a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1096%2Ffj.02-0967fje$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1096%2Ffj.02-0967fje$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12709406$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Izzotti, Alberto</creatorcontrib><creatorcontrib>Balansky, Roumen M.</creatorcontrib><creatorcontrib>Cartiglia, Cristina</creatorcontrib><creatorcontrib>Camoirano, Anna</creatorcontrib><creatorcontrib>Longobardi, Mariagrazia</creatorcontrib><creatorcontrib>De Flora, Silvio</creatorcontrib><title>Genomic and transcriptional alterations in mouse fetus liver after transplacental exposure to cigarette smoke</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>ABSTRACT
The transplacental exposure of fetuses to maternal cigarette smoke may increase the risk of developmental impairments, congenital diseases, and childhood cancer. The whole‐body exposure of Swiss mice to environmental cigarette smoke (ECS) during pregnancy decreased the number of fetuses per dam, placenta weight, and fetus weight. ECS increased DNA adducts, oxidative nucleotide alterations, and cytogenetic damage in fetus liver. Evaluation by cDNA array of 746 genes showed that 61 of them were expressed in fetus liver under basal conditions. The oral administration of N‐acetylcysteine (NAC) during pregnancy enhanced the expression of three genes only, including two glutathione S‐transferases and α1‐antitrypsin precursor, whose deficiency plays a pathogenetic role in congenital emphysema. Transplacental ECS upregulated the expression of 116 genes involved in metabolism, response to oxidative stress, DNA and protein repair, and signal transduction. NAC inhibited the ECS‐related genetic damage and upregulation of most genes. ECS stimulated pro‐apoptotic genes and genes downregulating the cell cycle, which may justify growth impairments in the developing fetus. Thus, both genetic and epigenetic mechanisms were modulated by ECS. Moreover, hypoxia‐related genes and several oncogenes and receptors involved in proliferation and differentiation of leukocytes were induced in the fetal liver, which also bears hematopoietic functions.</description><subject>Acetylcysteine - pharmacology</subject><subject>Animals</subject><subject>Anticarcinogenic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Cell Hypoxia</subject><subject>DNA Adducts - metabolism</subject><subject>DNA Repair</subject><subject>Female</subject><subject>Fetus - anatomy & histology</subject><subject>Fetus - drug effects</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genome</subject><subject>genomic alterations</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Hematopoietic Stem Cells - drug effects</subject><subject>Liver - drug effects</subject><subject>Liver - embryology</subject><subject>Liver - metabolism</subject><subject>Maternal Exposure</subject><subject>Mice</subject><subject>mouse liver development</subject><subject>multigene expression analysis</subject><subject>N‐acetylcysteine</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Parity - drug effects</subject><subject>Placenta - anatomy & histology</subject><subject>Placenta - drug effects</subject><subject>Pregnancy</subject><subject>Smoking - adverse effects</subject><subject>Transcription, Genetic</subject><subject>transplacental cigarette smoke</subject><issn>0892-6638</issn><issn>1530-6860</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDlPxDAUhC0EguUoaZEruizPTmIndIB2OYREAdSW4zwjL7mwHY5_T1a7Eh3Vm5G-GekNIacM5gxKcWFXc-DJpKRd4Q6ZsTyFRBQCdskMipInQqTFATkMYQUADJjYJweMSygzEDPS3mLXt85Q3dU0et0F490QXd_phuomotdrE6jraNuPAanFOAbauE_0VNsJ2MSGRhvs4pTC76EPo0cae2rcm_YYI9LQ9u94TPasbgKebO8ReV0uXm7uksen2_ubq8fEpJItEq55jcbooshkbkFWeVbJ1GSGMyysAFPXNeaVNcaUWSnQyqowjEPJcsYynadH5HzTO_j-Y8QQVeuCwabRHU5PKCZZymQhJzDZgMb3IXi0avCu1f5HMVDrfZVdKeBqu-_En22Lx6rF-o_eDjoBlxvgyzX483-bWj5f8-UD8LVfPizSXyAdjDc</recordid><startdate>200306</startdate><enddate>200306</enddate><creator>Izzotti, Alberto</creator><creator>Balansky, Roumen M.</creator><creator>Cartiglia, Cristina</creator><creator>Camoirano, Anna</creator><creator>Longobardi, Mariagrazia</creator><creator>De Flora, Silvio</creator><general>Federation of American Societies for Experimental Biology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>200306</creationdate><title>Genomic and transcriptional alterations in mouse fetus liver after transplacental exposure to cigarette smoke</title><author>Izzotti, Alberto ; Balansky, Roumen M. ; Cartiglia, Cristina ; Camoirano, Anna ; Longobardi, Mariagrazia ; De Flora, Silvio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371E-2a2decca88475f07b54b73c4c21e8f60cddde5bfccc9496ef7b8c120915114a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acetylcysteine - pharmacology</topic><topic>Animals</topic><topic>Anticarcinogenic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Cell Hypoxia</topic><topic>DNA Adducts - metabolism</topic><topic>DNA Repair</topic><topic>Female</topic><topic>Fetus - anatomy & histology</topic><topic>Fetus - drug effects</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genome</topic><topic>genomic alterations</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>Hematopoietic Stem Cells - drug effects</topic><topic>Liver - drug effects</topic><topic>Liver - embryology</topic><topic>Liver - metabolism</topic><topic>Maternal Exposure</topic><topic>Mice</topic><topic>mouse liver development</topic><topic>multigene expression analysis</topic><topic>N‐acetylcysteine</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Parity - drug effects</topic><topic>Placenta - anatomy & histology</topic><topic>Placenta - drug effects</topic><topic>Pregnancy</topic><topic>Smoking - adverse effects</topic><topic>Transcription, Genetic</topic><topic>transplacental cigarette smoke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Izzotti, Alberto</creatorcontrib><creatorcontrib>Balansky, Roumen M.</creatorcontrib><creatorcontrib>Cartiglia, Cristina</creatorcontrib><creatorcontrib>Camoirano, Anna</creatorcontrib><creatorcontrib>Longobardi, Mariagrazia</creatorcontrib><creatorcontrib>De Flora, Silvio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>The FASEB journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Izzotti, Alberto</au><au>Balansky, Roumen M.</au><au>Cartiglia, Cristina</au><au>Camoirano, Anna</au><au>Longobardi, Mariagrazia</au><au>De Flora, Silvio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genomic and transcriptional alterations in mouse fetus liver after transplacental exposure to cigarette smoke</atitle><jtitle>The FASEB journal</jtitle><addtitle>FASEB J</addtitle><date>2003-06</date><risdate>2003</risdate><volume>17</volume><issue>9</issue><spage>1127</spage><epage>1129</epage><pages>1127-1129</pages><issn>0892-6638</issn><eissn>1530-6860</eissn><abstract>ABSTRACT
The transplacental exposure of fetuses to maternal cigarette smoke may increase the risk of developmental impairments, congenital diseases, and childhood cancer. The whole‐body exposure of Swiss mice to environmental cigarette smoke (ECS) during pregnancy decreased the number of fetuses per dam, placenta weight, and fetus weight. ECS increased DNA adducts, oxidative nucleotide alterations, and cytogenetic damage in fetus liver. Evaluation by cDNA array of 746 genes showed that 61 of them were expressed in fetus liver under basal conditions. The oral administration of N‐acetylcysteine (NAC) during pregnancy enhanced the expression of three genes only, including two glutathione S‐transferases and α1‐antitrypsin precursor, whose deficiency plays a pathogenetic role in congenital emphysema. Transplacental ECS upregulated the expression of 116 genes involved in metabolism, response to oxidative stress, DNA and protein repair, and signal transduction. NAC inhibited the ECS‐related genetic damage and upregulation of most genes. ECS stimulated pro‐apoptotic genes and genes downregulating the cell cycle, which may justify growth impairments in the developing fetus. Thus, both genetic and epigenetic mechanisms were modulated by ECS. Moreover, hypoxia‐related genes and several oncogenes and receptors involved in proliferation and differentiation of leukocytes were induced in the fetal liver, which also bears hematopoietic functions.</abstract><cop>United States</cop><pub>Federation of American Societies for Experimental Biology</pub><pmid>12709406</pmid><doi>10.1096/fj.02-0967fje</doi><tpages>24</tpages></addata></record> |
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| subjects | Acetylcysteine - pharmacology Animals Anticarcinogenic Agents - pharmacology Apoptosis Cell Cycle - drug effects Cell Division - drug effects Cell Hypoxia DNA Adducts - metabolism DNA Repair Female Fetus - anatomy & histology Fetus - drug effects Gene Expression Regulation - drug effects Genome genomic alterations Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - drug effects Liver - drug effects Liver - embryology Liver - metabolism Maternal Exposure Mice mouse liver development multigene expression analysis N‐acetylcysteine Oxidation-Reduction Oxidative Stress Parity - drug effects Placenta - anatomy & histology Placenta - drug effects Pregnancy Smoking - adverse effects Transcription, Genetic transplacental cigarette smoke |
| title | Genomic and transcriptional alterations in mouse fetus liver after transplacental exposure to cigarette smoke |
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