Maternal exposure to bisphenol A during pregnancy interferes ovaries development of F1 female mice

2020 ◽  
Vol 142 ◽  
pp. 138-148 ◽  
Author(s):  
Yuanyuan Wei ◽  
Chao Han ◽  
Shuying Li ◽  
Yuqing Cui ◽  
Yongzhan Bao ◽  
...  
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.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
K. M. Sujan ◽  
E. Haque ◽  
M. S. Rakib ◽  
M. I. Haque ◽  
A. Mustari ◽  
...  

Background: Bisphenol-A [BPA, 2, 2-bis (hydroxyphenyl) propane] is widely used in the manufacture of polycarbonate plastic, water bottles, feeders , baby bottles, epoxy resins and inside coating in metallic food cans. Black seed oil (BSO) (Nigella sativa) commonly known as black cumin, reported to be beneficial in function of various systems in the body. The study was carried out to investigate the effect of BPA and BSO on body weight, lipid profile and serum glucose in male and female mice. Methods : A total of thirty (15 male and 15 female) Swiss Albino mice (Mus musculus), aged 25-28 days with an average body weight of 27.4±1g were randomly divided into 3 groups consisting 5 mice in each for each sex. Group A served as vehicle control. Group B was administered BPA @ 50 mg/kg bw daily, while group C received both BPA @ 50 mg/kg/day and BSO @ 1ml/kg/day respectively. Results: Data revealed that BPA treated mice showed slight increase in body weight gain while BSO controlled the weight gain in BPA treated mice. Cholesterol and LDL values were significantly (p<0.01) increased and Triglycerides value was significantly (p<0.01) decreased in BPA-treated mice without significant alterations in HDL value. BPA & BSO treated female mice showed significant (p<0.01) decreased in cholesterol, triglycerides and LDL values. BPA reduced the blood glucose level and addition of BSO had synergistic effects of glucose utilization. Conclusions: It can be concluded that BPA is one of the potential risk factors for hyperlipidemia and obesity. These harmful effects could be alleviated by the ingestion of black seed oil.


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 ◽  
2012 ◽  
Vol 296 (1-3) ◽  
pp. 73-82 ◽  
Author(s):  
Young Jung Jang ◽  
Hee Ra Park ◽  
Tae Hyung Kim ◽  
Wook-Jin Yang ◽  
Jong-Joo Lee ◽  
...  

2002 ◽  
Vol 16 (2) ◽  
pp. 107-116 ◽  
Author(s):  
Atsuko Suzuki ◽  
Akika Sugihara ◽  
Kaoru Uchida ◽  
Tomomi Sato ◽  
Yasuhiko Ohta ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Takeshi Yamamoto ◽  
Yuma Tsubota ◽  
Toshihisa Kodama ◽  
Natsuko Kageyama-Yahara ◽  
Makoto Kadowaki

We examined whether maternal exposure to food antigens during lactation and maternal allergic status would affect the development of food allergy in offspring. OVA-sensitized or OVA-nonsensitized BALB/c female mice were exposed or unexposed to OVA during lactation. After weaning, their offspring were systemically sensitized twice with OVA and repeatedly given OVA by oral intubation. While 97.1% of the mice breastfed by OVA-nonsensitized and OVA-unexposed mothers developed allergic diarrhea, 59.7% of the mice breastfed by OVA-exposed nonallergic mothers during lactation and 24.6% of the mice breastfed by OVA-exposed allergic mothers during lactation developed food allergy. Furthermore, OVA was detected in breast-milk from OVA-exposed nonallergic mothers during lactation (4.6±0.5 μg/mL). In addition, OVA-specific IgG1 titers were markedly increased in breast milk from allergic mothers (OVA-sensitized and OVA-unexposed mother:11.0±0.5, OVA-sensitized and OVA-exposed mother:12.3±0.3). Our results suggest that oral tolerance induced by breast milk-mediated transfer of dietary antigens along with their specific immunoglobulins to offspring leads to antigen-specific protection from food allergy.


2012 ◽  
Vol 87 (4) ◽  
Author(s):  
Katherine E. Brannick ◽  
Zelieann R. Craig ◽  
Ashley D. Himes ◽  
Jackye R. Peretz ◽  
Wei Wang ◽  
...  

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