Associations between Maternal Exposure to Bisphenol A or Triclosan and Gestational Hypertension and Preeclampsia: The MIIREC Study

2018 ◽  
Vol 2018 (1) ◽  
Author(s):  
Louopou Rosalie Camara ◽  
Tye Arbuckle ◽  
Helen Trottier ◽  
William Fraser
2014 ◽  
Vol 220 (3) ◽  
pp. 375-388 ◽  
Author(s):  
Lydie Naulé ◽  
Marie Picot ◽  
Mariangela Martini ◽  
Caroline Parmentier ◽  
Hélène Hardin-Pouzet ◽  
...  

Bisphenol A (BPA) is a widespread estrogenic compound. We investigated the effects of maternal exposure to BPA at reference doses on sexual behavior and neuroendocrine functions of female offspring in C57BL/6J mice. The dams were orally exposed to vehicle alone or vehicle-containing BPA at doses equivalent to the no observed adverse effect level (5 mg/kg body weight per day) and tolerable daily intake (TDI, 0.05 mg/kg body weight per day) level from gestational day 15 until weaning. Developmental exposure to BPA increased the lordosis quotient in naive females exposed to BPA at the TDI dose only. BPA exposure had no effect on olfactory preference, ability to express masculine behaviors or number of calbindin-positive cells, a sexually dimorphic population of the preoptic area. BPA at both doses selectively increased kisspeptin cell number in the preoptic periventricular nucleus of the rostral periventricular area of the third ventricle in adult females. It did not affect the number of GNRH-positive cells or percentage of kisspeptin appositions on GNRH neurons in the preoptic area. These changes were associated with higher levels of estradiol (E2) at the TDI dose while levels of LH, estrus cyclicity, ovarian and uterine weights, and fertility remained unaffected. Delay in the time of vaginal opening was observed during the postnatal period at TDI dose, without any alteration in body growth. This shows that developmental exposure to BPA at reference doses did not masculinize and defeminize the neural circuitry underlying sexual behavior in female mice. The TDI dose specifically exacerbated responses normally induced by ovarian E2, through estrogen receptor α, during the postnatal/prepubertal period.


Toxicology ◽  
2020 ◽  
Vol 432 ◽  
pp. 152393 ◽  
Author(s):  
Haibin Zhang ◽  
Zhouyu Wang ◽  
Lingxue Meng ◽  
Hongxuan Kuang ◽  
Jian Liu ◽  
...  

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.


Toxicology ◽  
2014 ◽  
Vol 322 ◽  
pp. 51-60 ◽  
Author(s):  
Chong Wang ◽  
Ruiyan Niu ◽  
Yuchen Zhu ◽  
Haijun Han ◽  
Guangying Luo ◽  
...  

2012 ◽  
Vol 110 (2) ◽  
pp. 537-542 ◽  
Author(s):  
C. S. Rosenfeld ◽  
P. T. Sieli ◽  
D. A. Warzak ◽  
M. R. Ellersieck ◽  
K. A. Pennington ◽  
...  

Author(s):  
Mohammad Mehdi Amin ◽  
Zahra Ghasemi ◽  
Mehri Khoshhali ◽  
Ensiyeh Taheri ◽  
Bahare Dehdashti ◽  
...  

2021 ◽  
pp. 074823372098462
Author(s):  
Chong Wang ◽  
Yao Shu ◽  
Li Xu ◽  
Qiling Liu ◽  
Bei Zhang ◽  
...  

Bisphenol A (BPA), a component of polycarbonate and epoxy resins, has been reported to induce learning and memory deficits. However, the mechanisms have not been fully elucidated. Growing evidence has suggested that N-methyl-d-aspartate receptors (NMDARs) are involved in cognitive impairments. In this study, BPA was administered to female Sprague–Dawley rats (six per dose group) at concentrations of 0 (control), 4, 40, and 400 μg/kg·body weight/day from gestation day 1 through lactation day 21. Spatial learning was evaluated using the Morris water maze on postnatal day 22. Expression levels of NMDARs were determined using real-time polymerase chain reaction and Western blot. The results showed that male offspring exposed to BPA exhibited increased latency in reaching the platform and reduced time in the target quadrant, and the number of crossing the platform was less, as compared with the control group. The mRNA and protein expression levels of NMDARs in the hippocampus were significantly downregulated when compared with the control group of male offspring. The data showed that maternal exposure to BPA at low dosage can cause cognitive deficits in male rat offspring, probably due to a decrease in NMDARs in the hippocampus.


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