Neuroendocrine disruption of pubertal timing and interactions between homeostasis of reproduction and energy balance

Bourguignon, Jean-Pierre; Rasier, Grégory; Lebrethon, Marie-Christine; Gérard, Arlette; Naveau, Elise; Parent, Anne-Simone

doi:10.1016/j.mce.2010.02.033

Cited by 50 publications

(29 citation statements)

References 117 publications

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“…However, it is possible that such mechanisms ultimately affect the timing of puberty. Ultimately, such data in fish might contribute to our understanding of effects in Downloaded by [University of New Mexico] at 09:00 01 December 2014 human populations and notably the increased rate of sexual precocity observed in girls after migration (Bourguignon et al 2010); however, this will require more thorough investigations. An important issue that needs to be studied is the potential adverse effects of low doses and mixtures of EDC on GnRH and Kiss neuronal development and activity.…”

Section: Conclusion: Edc Have the Potential To Affect Brain Sexual Dmentioning

confidence: 99%

“…While this certainly holds true in fish, there are nevertheless an increasing number of studies focusing on how EDC may affect the neuroendocrine system of teleost fish, and the aim of this review was to synthesize this information that predominantly relates to reproduction. For effects on mammalian species, there are recent reviews available (Gore 2010;Bourguignon et al 2010;Diamanti-Kandarakis et al 2009;Crews et al 2007).…”

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confidence: 99%

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Neuroendocrine Effects of Endocrine Disruptors in Teleost Fish

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Vosges

Servili

et al. 2011

Journal of Toxicology and Environmental Health, Part B

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Because a large proportion of potential endocrine disruptors (EDC) end up in surface waters, aquatic species are particularly vulnerable to their potential adverse effects. Recent studies identified a number of brain targets for EDC commonly present in environmentally relevant concentrations in surface waters. Among those neuronal systems disrupted by EDC are the gonadotropin-releasing hormone (GnRH) neurons, the dopaminergic and serotoninergic circuits, and more recently the Kiss/GPR54 system, which regulates gonadotropin release. However, one of the most striking effects of EDC, notably estrogen mimics, is their impact on the cyp19a1b gene that encodes the brain aromatase isoform in fish. Moreover, this is the only example in which the molecular basis of endocrine disruption is fully understood. The aims of this review were to (1) synthesize the most recent discoveries concerning the EDC effects upon neuroendocrine systems of fish and (2) provide, when possible, the underlying molecular basis of disruption for each system concerned. The potential adverse effects of EDC on neurogenesis, puberty, and brain sexualization are also described. It is important to point out the future environmental, social, and economical issues arising from endocrine disruption studies in the context of risk assessment.

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Section: Conclusion: Edc Have the Potential To Affect Brain Sexual Dmentioning

confidence: 99%

mentioning

confidence: 99%

Neuroendocrine Effects of Endocrine Disruptors in Teleost Fish

Page

Vosges

Servili

et al. 2011

Journal of Toxicology and Environmental Health, Part B

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“…Developmental exposures to estrogenic EDCs alter many neuroendocrine reproductive functions [11;12]. BPA and other estrogenic EDCs (diethylstilbestrol (DES), methoxychlor (MXC)) are reported to alter the timing of puberty onset [11-15], however not consistently [16;17].…”

Section: Introductionmentioning

confidence: 99%

Regulation of arcuate genes by developmental exposures to endocrine-disrupting compounds in female rats

Roepke

Yang

Yasrebi

et al. 2016

Reproductive Toxicology

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Developmental exposure to endocrine-disrupting compounds (EDCs) alters reproduction and energy homeostasis, both of which are regulated by the arcuate nucleus (ARC). Little is known about the effects of EDC on ARC gene expression. In Experiment #1, pregnant dams were treated with either two doses of bisphenol A (BPA) or oil from embryonic day (E)18-21. Neonates were injected from postnatal day (PND)0-7. Vaginal opening, body weights, and ARC gene expression were measured. Chrm3 (muscarinic receptor 3) and Adipor1 (adiponectin receptor 1) were decreased by BPA. Bdnf (brain-derived neurotropic factor), Igf1 (insulin-like growth factor 1), Htr2c (5-hydroxytryptamine receptor), and Cck2r (cholescystokinin 2 receptor) were impacted. In Experiment #2, females were exposed to BPA, diethylstilbestrol (DES), di(2-ethylhexyl)phthalate, or methoxychlor (MXC) during E11-PND7. MXC and DES advanced the age of vaginal opening and ARC gene expression was impacted. These data indicate that EDCs alter ARC genes involved in reproduction and energy homeostasis in females.

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“…The physiological effects of BPA on adults are well documented, but the mode of BPA action on the developing brain has yet to be defined clearly, especially in the hypothalamus, which plays a known role in neuroendocrine disorders that are on the rise, including obesity and precocious puberty, as well as anxiety and hyperactivity (1,2,4,10,22). BPA is commonly thought to exert its effects by acting as a weak estrogen receptor (ER) agonist (8), although antagonism at androgen receptors (ARs) and thyroid receptors (ThRs) has been shown also (23).…”

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confidence: 99%

Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish

Kinch

Ibhazehiebo

Jeong

et al. 2015

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

406

255

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Bisphenol A (BPA), a ubiquitous endocrine disruptor that is present in many household products, has been linked to obesity, cancer, and, most relevant here, childhood neurological disorders such as anxiety and hyperactivity. However, how BPA exposure translates into these neurodevelopmental disorders remains poorly understood. Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 μM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPAmediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise.endocrine disruption | androgen receptor | aromatase | hyperactivity I n humans and rodent models, gestational exposure to bisphenol A (BPA) has been associated with increased risk of developing social (e.g., aggression), psychiatric (e.g., depression), and behavioral (e.g., hyperactivity) challenges later in life (1-7). BPA is a compound used in the production of diverse consumer products, ranging from baby bottles to thermal paper used for credit card receipts (8-10). Even though adults can experience adverse health following continued exposure to BPA, the fetal brain is especially vulnerable because of an immature xenobioticmetabolizing system and blood-brain barrier (11,12). Exactly how BPA exposure in utero translates into neurodevelopmental disorders later in life is only beginning to be explored (13-15).Despite a wide body of research illustrating adverse effects of BPA, controversy exists around the true effects of low-dose exposure, as is most often the case in humans. In accordance with standardized toxicological testing procedures, government agencies in the United States (the US Environmental Protection Agency, USEPA), Canada (Health Canada), and Europe (the European Food Safety Authority, EFSA) have established tolerable daily intake levels, ranging from 25-50 μg BPA·kg body weight [16][17][18]. Given th...

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Neuroendocrine disruption of pubertal timing and interactions between homeostasis of reproduction and energy balance

Cited by 50 publications

References 117 publications

Neuroendocrine Effects of Endocrine Disruptors in Teleost Fish

Neuroendocrine Effects of Endocrine Disruptors in Teleost Fish

Regulation of arcuate genes by developmental exposures to endocrine-disrupting compounds in female rats

Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish

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