Pubertal timing after neonatal diethylstilbestrol exposure in female rats: Neuroendocrine vs peripheral effects and additive role of prenatal food restriction

Franssen, Delphine; Ioannou, Yiannis; Alvarez-Real, Alexandra; Gérard, Arlette; Mueller, Johanna K.; Heger, Sabine; Bourguignon, Jean-Pierre; Parent, Anne-Simone

doi:10.1016/j.reprotox.2013.10.006

Cited by 38 publications

(37 citation statements)

References 56 publications

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“…This part of our study demonstrating significant alteration of pubertal timing suggests interference of NP PEG-b-PLA with the neuroendocrine system as it is consistent with recent records of ED effects [39,42].…”

Section: Discussionsupporting

confidence: 92%

“…A low dose of NP (intratracheally, 11 μg/animal) elicited significantly earlier onset of puberty in female offspring compared to controls, while this effect was not observed in higher dose groups (54 and 268 μg/animal) [20]. Our results are consistent with the results of recent studies demonstrating that critical perinatal exposure to EDs accelerates the pubertal onset in the female rodents and that timing of the exposure, doses, and response stages of specific tissues are critical [10,11,20,[35][36][37][38][39][40].…”

Section: Discussionsupporting

confidence: 92%

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Delayed adverse effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether on hypothalamic–pituitary–ovarian axis development and function in Wistar rats

Rollerová

Jurčovičová

Mlynarčíková

et al. 2015

Reproductive Toxicology

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Delayed adverse effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether on hypothalamic–pituitary–ovarian axis development and function in Wistar rats

Rollerová

Jurčovičová

Mlynarčíková

et al. 2015

Reproductive Toxicology

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“…The purpose of the present study was to further elucidate the impact of the dose of BPA on female puberty and the underlying neuroendocrine mechanism with emphasis on rat exposure to low environmentally relevant doses during the early postnatal window. The mechanistic issue was addressed using an ex vivo paradigm of pulsatile GnRH secretion from hypothalamic explants (16) that was shown to be affected by other EDCs in previous studies (17,18).…”

mentioning

confidence: 99%

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

et al. 2016

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Rat sexual maturation is preceded by a reduction of the interpulse interval (IPI) of GnRH neurosecretion. This work aims at studying disruption of that neuroendocrine event in females after early exposure to a very low dose of bisphenol A (BPA), a ubiquitous endocrine disrupting chemical. Female rats were exposed to vehicle or BPA 25 ng/kg·d, 25 μg/kg·d, or 5 mg/kg·d from postnatal day (PND)1 to PND5 or PND15. Exposure to 25 ng/kg·d of BPA for 5 or 15 days was followed by a delay in developmental reduction of GnRH IPI studied ex vivo on PND20. After 15 days of exposure to that low dose of BPA, vaginal opening tended to be delayed. In contrast, exposure to BPA 5 mg/kg·d for 15 days resulted in a premature reduction in GnRH IPI and a trend toward early vaginal opening. RNA sequencing analysis on PND20 indicated that exposure to BPA resulted in opposing dose effects on the mRNA expression of hypothalamic genes involved in gamma aminobutyric acid A (GABAA) neurotransmission. The study of GnRH secretion in vitro in the presence of GABAA receptor agonist/antagonist confirmed an increased or a reduced GABAergic tone after in vivo exposure to the very low or the high dose of BPA, respectively. Overall, we show for the first time that neonatal exposure to BPA leads to opposing dose-dependent effects on the neuroendocrine control of puberty in the female rat. A very low and environmentally relevant dose of BPA delays neuroendocrine maturation related to puberty through increased inhibitory GABAergic neurotransmission.

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“…And the most of estrogenic compounds considered to be accelerated rather than delayed puberty in the rodents by prenatal or prepubertal exposure. However, it was recently suggested that neonatal subcutaneous exposure to 1 g/kg of DES delayed female puberty in rats [22]. Thus, changes in female puberty are not necessarily accelerated with neonatal DES exposure.…”

Section: Discussionmentioning

confidence: 98%

Ovarian dysfunction, obesity and pituitary tumors in female mice following neonatal exposure to low-dose diethylstilbestrol

Ohta

Ohmukai

Toyoizumi

et al. 2014

Reproductive Toxicology

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Pubertal timing after neonatal diethylstilbestrol exposure in female rats: Neuroendocrine vs peripheral effects and additive role of prenatal food restriction

Cited by 38 publications

References 56 publications

Delayed adverse effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether on hypothalamic–pituitary–ovarian axis development and function in Wistar rats

Delayed adverse effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether on hypothalamic–pituitary–ovarian axis development and function in Wistar rats

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

Ovarian dysfunction, obesity and pituitary tumors in female mice following neonatal exposure to low-dose diethylstilbestrol

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