THE UNIQUE PHARMACOKINETIC CHARACETERISTICS OF BISPHENOL A IN AMNIOTIC FLUID: THE IMPLICATION OF FETAL EXPOSURE

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Chensheng (Alex) Lu ◽  
Andrea Edlow ◽  
Nicole Smith ◽  
Mei Chen ◽  
Thomas McElrath
2016 ◽  
Vol 86 ◽  
pp. 52-59 ◽  
Author(s):  
Glenn Gauderat ◽  
Nicole Picard-Hagen ◽  
Pierre-Louis Toutain ◽  
Tanguy Corbel ◽  
Catherine Viguié ◽  
...  

2020 ◽  
Vol 136 ◽  
pp. 105407 ◽  
Author(s):  
Bo Zhang ◽  
Yuan He ◽  
Hongkai Zhu ◽  
Xiongfei Huang ◽  
Xueyuan Bai ◽  
...  

2019 ◽  
Vol 47 (7) ◽  
pp. 765-770 ◽  
Author(s):  
Monika Zbucka-Krętowska ◽  
Urszula Łazarek ◽  
Wojciech Miltyk ◽  
Iwona Sidorkiewicz ◽  
Piotr Pierzyński ◽  
...  

Abstract Background Bisphenol A (BPA) is an estrogenic, endocrine-disrupting compound widely used in the industry. It is also a ubiquitous environmental pollutant. Its presence was confirmed in human fetuses, which results from maternal exposure during pregnancy. The mechanisms behind maternal-fetal transfer, and relationships between pregnant women and fetal exposures remain unclear. The aim of this study was to assess the impact of maternal exposure to BPA on the exposure of the fetus. Methods Maternal plasma and amniotic fluid samples were collected from 52 pregnant women undergoing amniocentesis for prenatal diagnosis of chromosomal abnormalities. BPA was measured by gas chromatography-mass spectrometry (GC-MS). The permeability factor – a ratio of fetal-to-maternal BPA concentration – was used as a measure delineating the transplacental transfer of BPA. Results The median concentration of maternal plasma BPA was 8 times higher than the total BPA concentration in the amniotic fluid (8.69 ng/mL, range: 4.3 ng/mL–55.3 ng/mL vs. median 1.03 ng/mL, range: 0.3 ng/mL–10.1 ng/mL). There was no direct relationship between the levels of BPA in maternal plasma and amniotic fluid levels. The permeability factor, in turn, negatively correlated with fetal development (birth weight) (R = −0.54, P < 0.001). Conclusion Our results suggest that the risk of fetal BPA exposure depends on placental BPA permeability rather than the levels of maternal BPA plasma concentration and support general recommendations to become aware and avoid BPA-containing products.


2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Kenichiro Ishii ◽  
Shigeki Arase ◽  
Yuko Yoshio ◽  
Katsuhide Igarashi ◽  
Kenichi Aisaki ◽  
...  

2020 ◽  
Author(s):  
Sonia Abdallah ◽  
Delphine Moison ◽  
Margaux Wieckowski ◽  
Sébastien Messiaen ◽  
Emmanuelle Martini ◽  
...  

SummaryMany endocrine disruptors have been proven to impair the meiotic process that is mandatory to produce healthy gametes. Bisphenol A is emblematic as it impairs meiotic prophase I and causes oocyte aneuploidy following in utero exposure. However, the mechanisms underlying these deleterious effects remain poorly understood. Furthermore, the increasing uses of BPA analogs raise concerns for public health. Here, we investigated the effect on oogenesis in mouse of fetal exposure to two BPA analogs, Bisphenol A Diglycidyl Ether (BADGE) or Bisphenol AF (BPAF). These analogs delay meiosis initiation, increase MLH1 foci per cell and induce oocyte aneuploidy. We further demonstrate that these defects are accompanied by a deregulation of gene expression and aberrant mRNA splicing in fetal premeiotic germ cells. Interestingly, we observed an increase in DNA oxidation after exposure to BPA analogs. Specific induction of oxidative DNA damages during fetal germ cell differentiation causes similar defects during oogenesis, as observed in 8-Oxoguanine DNA Glycosylase (OGG1) deficient mice or after in utero exposure to potassium bromate (KBrO3), an inducer of oxidative DNA damages. Moreover, the supplementation of N-acetylcysteine (NAC) with BPA analogs counteracts the bisphenol-induced meiotic effect. Together our results position oxidative stress as a central event that negatively impacts the female meiosis with major consequences on oocyte quality. This could be a common mechanism of action for so called endocrine disruptors pollutants and it could lead to novel strategies for reprotoxic compounds.


2005 ◽  
Vol 72 (6) ◽  
pp. 1344-1351 ◽  
Author(s):  
Caroline M. Markey ◽  
Perinaaz R. Wadia ◽  
Beverly S. Rubin ◽  
Carlos Sonnenschein ◽  
Ana M. Soto

2011 ◽  
Vol 34 (14) ◽  
pp. 1648-1655 ◽  
Author(s):  
Mei Chen ◽  
Andrea G. Edlow ◽  
Tao Lin ◽  
Nicole A. Smith ◽  
Thomas F. McElrath ◽  
...  

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