Effects of bisphenol A administration to pregnant mice on serum Ca and intestinal Ca absorption

2011 ◽  
Vol 83 (3) ◽  
pp. 232-237 ◽  
Author(s):  
Hinako OTSUKA ◽  
Miki SUGIMOTO ◽  
Shuntaro IKEDA ◽  
Shinichi KUME
2005 ◽  
Vol 87 (2) ◽  
pp. 199-213 ◽  
Author(s):  
Yuko Kawamoto ◽  
Wakoto Matsuyama ◽  
Masahiro Morikawa ◽  
Maki Morita ◽  
Miki Sugimoto ◽  
...  

2021 ◽  
Vol 22 (21) ◽  
pp. 11808
Author(s):  
Margaux Wieckowski ◽  
Stéphanie Ranga ◽  
Delphine Moison ◽  
Sébastien Messiaen ◽  
Sonia Abdallah ◽  
...  

For decades, numerous chemical pollutants have been described to interfere with endogenous hormone metabolism/signaling altering reproductive functions. Among these endocrine disrupting substances, Bisphenol A (BPA), a widely used compound, is known to negatively impact germ and somatic cells in the testis. Physical agents, such as ionizing radiation, were also described to perturb spermatogenesis. Despite the fact that we are constantly exposed to numerous environmental chemical and physical compounds, very few studies explore the impact of combined exposure to chemical and physical pollutants on reproductive health. The aim of this study was to describe the impact of fetal co-exposure to BPA and IR on testicular function in mice. We exposed pregnant mice to 10 µM BPA (corresponding to 0.5 mg/kg/day) in drinking water from 10.5 dpc until birth, and we irradiated mice with 0.2 Gy (γ-ray, RAD) at 12.5 days post-conception. Co-exposure to BPA and γ-ray induces DNA damage in fetal germ cells in an additive manner, leading to a long-lasting decrease in germ cell abundance. We also observed significant alteration of adult steroidogenesis by RAD exposure independently of the BPA exposure. This is illustrated by the downregulation of steroidogenic genes and the decrease of the number of adult Leydig cells. As a consequence, courtship behavior is modified, and male ultrasonic vocalizations associated with courtship decreased. In conclusion, this study provides evidence for the importance of broadening the concept of endocrine disruptors to include physical agents, leading to a reevaluation of risk management and regulatory decisions.


2013 ◽  
Vol 25 (1) ◽  
pp. 209
Author(s):  
S. Kim ◽  
E. B. Jeung

Octylphenol (OP) is a degradation product of alkylphenol ethoxylates that are widely used to in rubber, pesticides, and paints. Bisphenol A (BPA) is an organic compound with two functional phenol groups and used to make polycarbonate plastic and epoxy resins, along with other applications. OP and BPA are known as endocrine disruptors that can induce inappropriate estrogenic action, and may disturb natural calcium metabolism. In the present study, the effects of OP and BPA on the calcium levels of serum and urine, and calcium transport genes were investigated in the duodenum and kidney of the pregnant mice. From 6.5 to 16.5 days post-coitus (dpc), 5 pregnant mice for each group were orally given with ethylestradiol (EE, 0.2 mg kg–1 day –1), OP (15, 45, or 135 mg kg–1 day–1) or BPA (5 or 50 mg kg–1 day –1) dissolved in corn oil. The duodenum, kidney, blood, and urine were obtained from the mice at day 18.5 of pregnancy. As a result, serum and urinary calcium levels were decreased by OP and BPA in a dose-dependent manner. The mRNA expression levels of calcium transport genes TRPV6 and CaBP-9k were decreased in the kidney after treatment with OP and BPA, while duodenal expression of TRPV6 was reduced by a high dose of BPA. The protein levels of these genes showed similar pattern with those of mRNA in the kidney and duodenum. The data were analyzed using a one-way ANOVA. P < 0.05 was considered statistically significant. Taken together, OP and BPA altered gene expressions associated with calcium transport in the pregnant mice, which may cause reduced serum and urine calcium levels. These results suggest that estrogenic actions of OP and BPA may lead to influence the calcium levels during pregnancy in the mice.


2018 ◽  
Vol 33 (2) ◽  
pp. 2732-2742 ◽  
Author(s):  
Yunzhen Ye ◽  
Yao Tang ◽  
Yu Xiong ◽  
Liping Feng ◽  
Xiaotian Li

Author(s):  
Rebecca Whitehead ◽  
Haiyan Guan ◽  
Edith Arany ◽  
Maria Cernea ◽  
Kaiping Yang

AbstractExposure to bisphenol A (BPA), an endocrine disrupting chemical, during gestation is associated with a variety of metabolic dysfunctions in adulthood, including hyperinsulinemia, glucose intolerance and insulin resistance. These modifications in glucose homeostasis largely stem from alterations in pancreatic function. However, the effects of BPA on the fetal pancreas have never been explored. The present study addressed this important question by examining the effects of prenatal BPA exposure on the mouse fetal pancreatic development.Pregnant mice were fed a BPA diet (25 mg BPA/kg diet) from embryonic day 7.5 (E7.5) to E18.5. At E18.5, fetal pancreata were collected and analyzed for morphological changes in the endocrine pancreas such as islet size, number and β and α cell distribution.We showed that BPA exposed fetal pancreata had a greater number of islet-cell clusters (ICCs; <300 μmConsidering that ICCs represent the initial stages of islet development in the fetal pancreas, our findings suggest that BPA promotes islet differentiation or delays the conversion of ICCs into mature islets. Moreover, the increase in glucagon expression suggests a potential alteration in the α:β-cell ratio in islets, which may have significant implications for the fetal pancreas both structurally and functionally. This study provides novel insight into the effects of BPA exposure on the fetal pancreata, indicating alterations in glucagon expression in islets and ICCs.


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