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.
Environ Sci Technol. 2017 Jun 6;51(11):6422-6429. doi: 10.1021/acs.est.7b00801. Epub 2017 May 17.
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-NOGua)) as well as products of lipid peroxidation (8-iso-prostaglandin F (8-isoPF) 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-NOGua levels, between BPA and 8-isoPF 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.
产前暴露于壬基酚（NP）和/或双酚 A（BPA）与不良出生结局有关；然而，其潜在机制尚不清楚。主要机制是雌激素受体结合亲和力的内分泌干扰，但氧化应激和炎症也可能起作用。我们旨在研究 241 对母婴尿液 NP 和 BPA 水平与氧化/硝化应激和炎症生物标志物的关系，并探讨氧化/硝化应激的变化是否是 NP/BPA 产前暴露和炎症的功能。同时测量了第三孕期尿液氧化/硝化应激生物标志物，包括氧化和硝化损伤 DNA 的产物（8-羟基-2'-脱氧鸟苷（8-OHdG）和 8-硝基鸟嘌呤（8-NOGua））以及脂质过氧化产物（8-异前列腺素 F（8-isoPF）和 4-羟基-2-壬烯醛-巯基尿酸（HNE-MA））。分析了母体和脐带血浆样本中的抗氧化谷胱甘肽过氧化物酶（GPx）和炎症生物标志物，包括 C 反应蛋白（CRP）和一组细胞因子（白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α））。在调整后的模型中，我们观察到 NP 暴露与 8-OHdG 和 8-NOGua 水平、BPA 与 8-isoPF 水平以及母体 CRP 水平与 HNE-MA 水平之间存在显著正相关。此外，脐带血中的 BPA 和 TNF-α 水平与脐带血中的母体和 GPx 水平以及母体 TNF-α 水平与母体 GPx 水平呈负相关。这些结果支持 NP 和 BPA 暴露以及炎症可能在怀孕期间增加氧化/硝化应激和降低抗氧化活性方面发挥作用。
