Effect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus–pituitary–gonadal axis of CD-1 mice

Wei, Xi; Lee, Ckf; Yeung, William S.B.; Giesy, John P.; Wong, Ming Hung; Zhang, Xiaowei; Hecker, Markus; Wong, Chris K C

doi:10.1016/j.reprotox.2010.12.002

Cited by 204 publications

(136 citation statements)

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“…The studies administering BPA at the TDI dose to neonatal rats did not detect any significant effect on kisspeptin immunoreactivity in the anteroventral periventricular nucleus , Losa-Ward et al 2012. The observed increase in kisspeptin immunoreactive cells could be due to BPA-induced transcriptional regulation of Kiss1 because increased hypothalamic levels of Kiss mRNAs were observed following oral exposure to high doses (25-50 mg/kg) of gestational and lactational BPA in CD1 mice (Xi et al 2011).…”

Section: Discussionmentioning

confidence: 94%

“…BPA treatment had no effect on kisspeptin immunoreactive fiber density in the arcuate nucleus or on the number of GNRH neurons in the preoptic area. It is therefore possible that increased E 2 levels result, at least partly, from a change in the balance between negative-and positive-feedback responses at the hypothalamic portion of the HPG axis, although a direct effect of BPA on follicular steroidogenesis (Xi et al 2011) cannot be excluded. The observations that females developmentally exposed to BPA exhibited normal estrus cyclicity, ovarian and uterine weights, and were able to ovulate and produce offspring indicate that BPA-induced alterations did not interfere with the normal functioning of the HPG axis.…”

Section: Discussionmentioning

confidence: 99%

“…This diversity in effects could be related to factors including differences in mouse strains, BPA dose, and time of exposure. At the neuroanatomical level, only one study reported increased levels of Kiss1 and Gnrh mRNAs after exposure to high doses of oral BPA (Xi et al 2011). These genes code for kisspeptin and GNRH, two important neuropeptides for the central regulation of reproductive function throughout life and known targets of a variety of estrogeno-mimetic endocrine disruptors (Gore 2010, Tena-Sempere 2010, Franceschini & Desroziers 2013.…”

Section: Introductionmentioning

confidence: 99%

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Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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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 (E 2 ) 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 E 2 , through estrogen receptor a, during the postnatal/prepubertal period.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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“…For example, food restriction during the first trimester of human pregnancy frequently leads to adult onset of obesity, diabetes, hypertension, and other aspects of ill health (30-34), a phenomenon that has been reproduced in several animal models (35)(36)(37). In addition, in utero exposure of test animals to industrial chemicals that mimic the action of steroid hormones can also have serious, although sometimes subtle, consequences with regard to development of the genitalia, the brain, and other organ systems, and may also increase the frequency of adult diseases, including cancer (26,(38)(39)(40)(41)(42)(43). Hence, the claim that the viable yellow (A vy /a) mouse could serve as a biosensor (44) for exposure to EDC, and might even be used to study the ability of nutritional supplements to counteract such environmental insults, provided an exciting prospect for risk assessment and even dietary recommendations for pregnant women.…”

Section: Discussionmentioning

confidence: 99%

Maternal exposure to bisphenol A and genistein has minimal effect onA^vy/aoffspring coat color but favors birth of agouti over nonagouti mice

Rosenfeld

Sieli

Warzak

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Reports that maternal diet influences coat color in mouse offspring carrying the agouti A vy allele have received considerable attention because the range, from pseudoagouti (brown) to yellow, predicts adult health outcomes, especially disposition toward obesity and diabetes, in yellower mice. Bisphenol A (BPA), an endocrine-disrupting compound with estrogenic properties, fed to a/a dams harboring A vy /a conceptuses has been reported to induce a significant shift toward yellower mice, whereas consumption of either genistein (G) alone or in combination with BPA led to greater numbers of healthy, brown offspring. Groups of C57/B6 a/a females, which are nonagouti, were fed either a phytoestrogen-free control diet or one of six experimental diets: diets 1-3 contained BPA (50 mg, 5 mg, and 50 μg BPA/kg food, respectively); diet 4 contained G (250 mg/kg food); diet 5 contained G plus BPA (250 and 50 mg/kg food, respectively); and diet 6 contained 0.1 μg of ethinyl estradiol (EE)/kg food. Mice were bred to A vy /a males over multiple parities. In all, 2,824 pups from 426 litters were born. None of the diets provided any significant differences in relative numbers of brown, yellow, or intermediate coat color A vy /a offspring. However, BPA plus G (P < 0.0001) and EE diets (P = 0.005), but not the four others, decreased the percentage of black (a/a) to A vy /a offspring from the expected Mendelian ratio of 1:1. Data suggest that A vy /a conceptuses, which may possess a so-called "thrifty genotype," are at a competitive advantage over a/a conceptuses in certain uterine environments.endocrine disruption | pregnancy | viable yellow mouse | epigenetics | metabolic disease

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“…were collected from the frozen slices (2-mm thick) and stored at K80 8C until assay. The primer sequences of Kiss1, Gnrh, Era, Erb, and Gapdh mRNA were designed and RT-qPCR was performed as described previously (Xi et al 2011). Total RNA was extracted using Trizol reagent kit (Invitrogen) according to the manufacturer's instructions.…”

Section: Rt-qpcrmentioning

confidence: 99%

Bisphenol A enhances kisspeptin neurons in anteroventral periventricular nucleus of female mice

Wang¹,

Fei²,

Bai³

et al. 2014

Journal of Endocrinology

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Bisphenol-A (BPA), an environmental estrogen, adversely affects female reproductive health. However, the underlying mechanisms remain largely unknown. We found that oral administration (p.o.) of BPA (20 mg/kg) to adult female mice at proestrus, but not at estrus or diestrus, significantly increased the levels of plasma E 2 , LH and FSH, and Gnrh mRNA within 6 h. The administration of BPA at proestrus, but not at diestrus, could elevate the levels of Kiss1 mRNA and kisspeptin protein in anteroventral periventricular nucleus (AVPV) within 6 h. In contrast, the level of Kiss1 mRNA in arcuate nucleus (ARC) was hardly altered by BPA administration. In addition, at proestrus, a single injection (i.c.v.) of BPA dose-dependently enhanced the AVPV-kisspeptin expression within 6 h, this was sensitive to E 2 depletion by ovariectomy and an estrogen receptor a (ERa) antagonist. Similarly, the injection of BPA (i.c.v.) at proestrus could elevate the levels of plasma E 2 , LH, and Gnrh mRNA within 6 h in a dose-dependent manner, which was blocked by antagonists of GPR54 or ERa. Injection of BPA (i.c.v.) at proestrus failed to alter the timing and peak concentration of LH-surge generation. In ovariectomized mice, the application of E 2 induced a dose-dependent increase in the AVPV-Kiss1 mRNA level, indicating 'E 2 -induced positive feedback', which was enhanced by BPA injection (i.c.v.). The levels of Era (Esr1) and Erb (Esr2) mRNAs in AVPV and ARC did not differ significantly between vehicle-and BPA-treated groups. This study provides in vivo evidence that exposure of adult female mice to a low dose of BPA disrupts the hypothalamic-pituitary-gonadal reproductive endocrine system through enhancing AVPVkisspeptin expression and release. Key Words

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Effect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus–pituitary–gonadal axis of CD-1 mice

Cited by 204 publications

References 58 publications

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Maternal exposure to bisphenol A and genistein has minimal effect onA^vy/aoffspring coat color but favors birth of agouti over nonagouti mice

Bisphenol A enhances kisspeptin neurons in anteroventral periventricular nucleus of female mice

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Effect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus–pituitary–gonadal axis of CD-1 mice

Cited by 204 publications

References 58 publications

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Maternal exposure to bisphenol A and genistein has minimal effect onAvy/aoffspring coat color but favors birth of agouti over nonagouti mice

Bisphenol A enhances kisspeptin neurons in anteroventral periventricular nucleus of female mice

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Maternal exposure to bisphenol A and genistein has minimal effect onA^vy/aoffspring coat color but favors birth of agouti over nonagouti mice