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首页> 外文期刊>Environmental Science & Technology >Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study
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Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study

机译：产前壬基酚和双酚A的暴露和炎症是氧化/硝化应激的决定因素：一项台湾队列研究

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摘要

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 oxidativeitrative stress and inflammation and to explore whether changes in oxidativeitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidativeitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-nitro- guanine (8-NO_2Gua)) as well as products of lipid peroxidation (8-iso- prostaglandin F_(2a) (8-isoPF_(2a)) 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-a (TNF-a)), 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-NO_2Gua levels, between BPA and 8-isoPF_(2a) levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-a levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-a levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidativeitrative stress and decreasing antioxidant activity during pregnancy.
机译：据报道，产前暴露于壬基酚（NP）和/或双酚A（BPA）与不良的出生结局有关。但是，其潜在机制仍不清楚。主要机制是内分泌破坏对雌激素受体的结合亲和力，但氧化应激和炎症也可能起一定作用。我们旨在调查尿中NP和BPA水平与氧化/硝化应激和炎症的生物标志物的关系，并探讨氧化/硝化应激的变化是否是产前暴露于241对母亲/胎儿的NP / BPA和炎症的函数。同时测量了妊娠晚期氧化/氧化应激的尿液生物标志物，包括氧化和硝化损伤的DNA（8-羟基-2'-脱氧鸟苷（8-OHdG）和8-硝基鸟嘌呤（8-NO_2Gua））的产物。作为脂质过氧化作用的产物（8-异前列腺素F_（2a）（8-isoPF_（2a））和4-羟基-2-壬烯-巯基酸（HNE-MA））。在孕妇中分析了抗氧化剂谷胱甘肽过氧化物酶（GPx）和炎症生物标记物，包括C反应蛋白（CRP）和一组细胞因子（白介素6（IL-6）和肿瘤坏死因子-a（TNF-a））。和脐带血浆样本。在调整后的模型中，我们观察到NP暴露与8-OHdG和8-NO_2Gua水平之间，BPA和8-isoPF_（2a）水平之间以及孕妇CRP水平与HNE-MA水平之间存在显着的正相关。另外，脐带血中的BPA和TNF-a水平与母体和GPx水平成反比，而母体TNF-a水平与母体GPx水平成反比。这些结果支持在怀孕期间暴露于NP和BPA以及可能引起炎症，从而增加氧化/硝化应激并降低抗氧化活性。

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  • 来源
    《Environmental Science & Technology》 |2017年第11期|6422-6429|共8页
  • 作者

    Yu-Fang Huang; Pei-Wei Wang; Li-Wei Huang; Chun-Hao Lai; Winnie Yang; Kuen-Yuh Wu; Chensheng Alex Lu; Hsin-Chang Chen; Mei-Lien Chen;

  • 作者单位

    Institute of Environmental and Occupational Health Sciences, National Yang Ming University, Taipei, Taiwan,Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts United States;

    Institute of Environmental and Occupational Health Sciences, National Yang Ming University, Taipei, Taiwan,Department of Pediatrics, Taipei City Hospital, Heping Fuyou Branch, Taipei, Taiwan;

    Department of Obstetrics & Gynecology, Taipei City Hospital, Heping Fuyou Branch, Taipei, Taiwan;

    Institute of Environmental and Occupational Health Sciences, National Yang Ming University, Taipei, Taiwan;

    Division of Pediatrics, Taipei City Hospital, Yangming Branch, Taipei, Taiwan;

    Institute of Occupational Medicine and Industrial Hygiene, National Taiwan University, Taipei, Taiwan;

    Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts United States;

    Institute of Occupational Medicine and Industrial Hygiene, National Taiwan University, Taipei, Taiwan;

    Institute of Environmental and Occupational Health Sciences, National Yang Ming University, Taipei, Taiwan;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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