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Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study
Prenatal exposure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse birth outcomes; however, the underlying mechanisms remain unclear. The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and...
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Published in: | Environmental science & technology 2017-06, Vol.51 (11), p.6422-6429 |
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description | Prenatal exposure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse birth outcomes; however, the underlying mechanisms remain unclear. The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation might also play a contributory role. We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-nitroguanine (8-NO2Gua)) as well as products of lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)). The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers, including C-reactive protein (CRP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed in maternal and umbilical cord plasma samples. In adjusted models, we observed significant positive associations between NP exposure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2α levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-α levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-α levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/nitrative stress and decreasing antioxidant activity during pregnancy. |
doi_str_mv | 10.1021/acs.est.7b00801 |
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The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation might also play a contributory role. We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-nitroguanine (8-NO2Gua)) as well as products of lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)). The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers, including C-reactive protein (CRP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed in maternal and umbilical cord plasma samples. In adjusted models, we observed significant positive associations between NP exposure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2α levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-α levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-α levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/nitrative stress and decreasing antioxidant activity during pregnancy.</description><identifier>ISSN: 0013-936X</identifier><identifier>EISSN: 1520-5851</identifier><identifier>DOI: 10.1021/acs.est.7b00801</identifier><identifier>PMID: 28490175</identifier><language>eng</language><publisher>United States: American Chemical Society</publisher><subject>8-Hydroxydeoxyguanosine ; Adult ; Antioxidants ; Benzhydryl Compounds - toxicity ; Binding sites ; Biomarkers ; Bisphenol A ; C-reactive protein ; Cohort analysis ; Cohort Studies ; Cord blood ; Cytokines ; Damage ; Deoxyguanosine ; Deoxyribonucleic acid ; Disruption ; DNA ; DNA Damage ; Endocrine disruptors ; Estrogens ; Exposure ; Female ; Fetal Blood ; Fetuses ; Glutathione ; Glutathione peroxidase ; Human exposure ; Humans ; Inflammation ; Interleukin 6 ; Interleukins ; Lipid peroxidation ; Maternal Exposure ; Nonylphenol ; Oxidative Stress ; Peroxidase ; Peroxidation ; Phenols - toxicity ; Pregnancy ; Prenatal development ; Prenatal experience ; Prenatal exposure ; Prostaglandins ; Tumor Necrosis Factor-alpha - blood ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Umbilical cord</subject><ispartof>Environmental science & technology, 2017-06, Vol.51 (11), p.6422-6429</ispartof><rights>Copyright © 2017 American Chemical Society</rights><rights>Copyright American Chemical Society Jun 6, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a361t-bacac9da9834ac27ce804144e450cc5872f20f0bd01c0d2785bb3829771e85a23</citedby><cites>FETCH-LOGICAL-a361t-bacac9da9834ac27ce804144e450cc5872f20f0bd01c0d2785bb3829771e85a23</cites><orcidid>0000-0002-8349-0126</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28490175$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Yu-Fang</creatorcontrib><creatorcontrib>Wang, Pei-Wei</creatorcontrib><creatorcontrib>Huang, Li-Wei</creatorcontrib><creatorcontrib>Lai, Chun-Hao</creatorcontrib><creatorcontrib>Yang, Winnie</creatorcontrib><creatorcontrib>Wu, Kuen-Yuh</creatorcontrib><creatorcontrib>Lu, Chensheng Alex</creatorcontrib><creatorcontrib>Chen, Hsin-Chang</creatorcontrib><creatorcontrib>Chen, Mei-Lien</creatorcontrib><title>Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study</title><title>Environmental science & technology</title><addtitle>Environ. Sci. Technol</addtitle><description>Prenatal exposure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse birth outcomes; however, the underlying mechanisms remain unclear. The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation might also play a contributory role. We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-nitroguanine (8-NO2Gua)) as well as products of lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)). The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers, including C-reactive protein (CRP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed in maternal and umbilical cord plasma samples. In adjusted models, we observed significant positive associations between NP exposure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2α levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-α levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-α levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/nitrative stress and decreasing antioxidant activity during pregnancy.</description><subject>8-Hydroxydeoxyguanosine</subject><subject>Adult</subject><subject>Antioxidants</subject><subject>Benzhydryl Compounds - toxicity</subject><subject>Binding sites</subject><subject>Biomarkers</subject><subject>Bisphenol A</subject><subject>C-reactive protein</subject><subject>Cohort analysis</subject><subject>Cohort Studies</subject><subject>Cord blood</subject><subject>Cytokines</subject><subject>Damage</subject><subject>Deoxyguanosine</subject><subject>Deoxyribonucleic acid</subject><subject>Disruption</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Endocrine disruptors</subject><subject>Estrogens</subject><subject>Exposure</subject><subject>Female</subject><subject>Fetal Blood</subject><subject>Fetuses</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Human exposure</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukins</subject><subject>Lipid peroxidation</subject><subject>Maternal Exposure</subject><subject>Nonylphenol</subject><subject>Oxidative Stress</subject><subject>Peroxidase</subject><subject>Peroxidation</subject><subject>Phenols - toxicity</subject><subject>Pregnancy</subject><subject>Prenatal development</subject><subject>Prenatal experience</subject><subject>Prenatal exposure</subject><subject>Prostaglandins</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Umbilical cord</subject><issn>0013-936X</issn><issn>1520-5851</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp1kVFrFDEUhYNU7Fr73DcJ9EWQ2b1JZiYZ39a1aqG0ghX6NtzJZOiUmWRNMtr9B_5ss92tQqFPSTjfOfeSQ8gJgzkDzhaow9yEOJcNgAL2gsxYwSErVMEOyAyAiawS5c0heR3CHQBwAeoVOeQqr4DJYkb-fPPGYsSBXjq7Gda3xrqBom3pxz7sX0t6dr92YfImPCjnthtwHDH2ztKlN_STicaPvUUbA3Udvbrv26T-MovLPvqHG_0ekz18SGHX2P9Ga4KhK3frfEzS1G7ekJcdDsEc788j8uPz2fXqa3Zx9eV8tbzIUJQsZg1q1FWLlRI5ai61UZCzPDd5AVoXSvKOQwdNC0xDy6UqmkYoXknJjCqQiyPybpe79u7nlP6uHvugzTCkldwUaqYqqUCCEAk9fYLeucnbtF3NKp7zkpeiTNRiR2nvQvCmq9e-H9Fvagb1tqQ6lVRv3fuSkuPtPndqRtP-4x9bScD7HbB1_p_5TNxfKFGeEA</recordid><startdate>20170606</startdate><enddate>20170606</enddate><creator>Huang, Yu-Fang</creator><creator>Wang, Pei-Wei</creator><creator>Huang, Li-Wei</creator><creator>Lai, Chun-Hao</creator><creator>Yang, Winnie</creator><creator>Wu, Kuen-Yuh</creator><creator>Lu, Chensheng Alex</creator><creator>Chen, Hsin-Chang</creator><creator>Chen, Mei-Lien</creator><general>American Chemical Society</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>7QO</scope><scope>7ST</scope><scope>7T7</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8349-0126</orcidid></search><sort><creationdate>20170606</creationdate><title>Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study</title><author>Huang, Yu-Fang ; Wang, Pei-Wei ; Huang, Li-Wei ; Lai, Chun-Hao ; Yang, Winnie ; Wu, Kuen-Yuh ; Lu, Chensheng Alex ; Chen, Hsin-Chang ; Chen, Mei-Lien</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a361t-bacac9da9834ac27ce804144e450cc5872f20f0bd01c0d2785bb3829771e85a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>8-Hydroxydeoxyguanosine</topic><topic>Adult</topic><topic>Antioxidants</topic><topic>Benzhydryl Compounds - toxicity</topic><topic>Binding sites</topic><topic>Biomarkers</topic><topic>Bisphenol A</topic><topic>C-reactive protein</topic><topic>Cohort analysis</topic><topic>Cohort Studies</topic><topic>Cord blood</topic><topic>Cytokines</topic><topic>Damage</topic><topic>Deoxyguanosine</topic><topic>Deoxyribonucleic acid</topic><topic>Disruption</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>Endocrine disruptors</topic><topic>Estrogens</topic><topic>Exposure</topic><topic>Female</topic><topic>Fetal Blood</topic><topic>Fetuses</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Human exposure</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukins</topic><topic>Lipid peroxidation</topic><topic>Maternal Exposure</topic><topic>Nonylphenol</topic><topic>Oxidative Stress</topic><topic>Peroxidase</topic><topic>Peroxidation</topic><topic>Phenols - toxicity</topic><topic>Pregnancy</topic><topic>Prenatal development</topic><topic>Prenatal experience</topic><topic>Prenatal exposure</topic><topic>Prostaglandins</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Umbilical cord</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Yu-Fang</creatorcontrib><creatorcontrib>Wang, Pei-Wei</creatorcontrib><creatorcontrib>Huang, Li-Wei</creatorcontrib><creatorcontrib>Lai, Chun-Hao</creatorcontrib><creatorcontrib>Yang, Winnie</creatorcontrib><creatorcontrib>Wu, Kuen-Yuh</creatorcontrib><creatorcontrib>Lu, Chensheng Alex</creatorcontrib><creatorcontrib>Chen, Hsin-Chang</creatorcontrib><creatorcontrib>Chen, Mei-Lien</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Environment Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental science & technology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Yu-Fang</au><au>Wang, Pei-Wei</au><au>Huang, Li-Wei</au><au>Lai, Chun-Hao</au><au>Yang, Winnie</au><au>Wu, Kuen-Yuh</au><au>Lu, Chensheng Alex</au><au>Chen, Hsin-Chang</au><au>Chen, Mei-Lien</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study</atitle><jtitle>Environmental science & technology</jtitle><addtitle>Environ. Sci. Technol</addtitle><date>2017-06-06</date><risdate>2017</risdate><volume>51</volume><issue>11</issue><spage>6422</spage><epage>6429</epage><pages>6422-6429</pages><issn>0013-936X</issn><eissn>1520-5851</eissn><abstract>Prenatal exposure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse birth outcomes; however, the underlying mechanisms remain unclear. The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation might also play a contributory role. We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-nitroguanine (8-NO2Gua)) as well as products of lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)). The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers, including C-reactive protein (CRP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed in maternal and umbilical cord plasma samples. In adjusted models, we observed significant positive associations between NP exposure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2α levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-α levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-α levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/nitrative stress and decreasing antioxidant activity during pregnancy.</abstract><cop>United States</cop><pub>American Chemical Society</pub><pmid>28490175</pmid><doi>10.1021/acs.est.7b00801</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-8349-0126</orcidid></addata></record> |
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subjects | 8-Hydroxydeoxyguanosine Adult Antioxidants Benzhydryl Compounds - toxicity Binding sites Biomarkers Bisphenol A C-reactive protein Cohort analysis Cohort Studies Cord blood Cytokines Damage Deoxyguanosine Deoxyribonucleic acid Disruption DNA DNA Damage Endocrine disruptors Estrogens Exposure Female Fetal Blood Fetuses Glutathione Glutathione peroxidase Human exposure Humans Inflammation Interleukin 6 Interleukins Lipid peroxidation Maternal Exposure Nonylphenol Oxidative Stress Peroxidase Peroxidation Phenols - toxicity Pregnancy Prenatal development Prenatal experience Prenatal exposure Prostaglandins Tumor Necrosis Factor-alpha - blood Tumor necrosis factor-TNF Tumor necrosis factor-α Umbilical cord |
title | Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study |
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