Neuroendocrine systems as targets for environmental endocrine-disrupting chemicals

Gore, Andrea C.

doi:10.1016/j.fertnstert.2007.12.039

Cited by 29 publications

(20 citation statements)

References 18 publications

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“…However, the effects of pesticides on neuroendocrine axes have been less of a focus. There is good evidence that pesticides are neuroactive in vertebrates, and these chemicals have been shown to affect the expression of neuropeptides (Gore, 2002), alter the reuptake of neurotransmitters such as dopamine (DA) (Miller et al, 1999), and bind to receptors that regulate neuroendocrine signaling (Gore, 2008). We present some of the evidence for neuroendocrine disrupting effects of organopesticides that includes both organochlorines (OCPs) and organophosphates (OPs).…”

Section: Legacy Pesticides As Neuroendocrine Disruptorsmentioning

confidence: 99%

“…In the last few years, it has also become clear that a subset of pollutants and mass-produced chemicals have significant effects on neuroendocrine systems. Following earlier key initiatives on synthesizing the principles of neuroendocrine disruption (Gore, 2008; Gore and Patisaul, 2010; Zoeller, 2008), a formal definition emerged following the first Symposium on Neuroendocrine Effects of Endocrine Disruptors in July 2010 (Trudeau et al, 2011). At that time, experimental evidence obtained from both invertebrate and vertebrate model systems was reviewed (Waye and Trudeau, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Current concepts in neuroendocrine disruption

León-Olea

Martyniuk

Orlando

et al. 2014

General and Comparative Endocrinology

126

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In the last few years, it has become clear that a wide variety of environmental contaminants have specific effects on neuroendocrine systems in fish, amphibians, birds and mammals. While it is beyond the scope of this review to provide a comprehensive examination of all of these neuroendocrine disruptors, we will focus on select representative examples. Organochlorine pesticides bioaccumulate in neuroendocrine areas of the brain that directly regulate GnRH neurons, thereby altering the expression of genes downstream of GnRH signaling. Organochlorine pesticides can also agonize or antagonize hormone receptors, adversely affecting crosstalk between neurotransmitter systems. The impacts of polychlorinated biphenyls are varied and in many cases subtle. This is particularly true for neuroedocrine and behavioral effects of exposure. These effects impact sexual differentiation of the hypothalamic-pituitary-gonadal axis, and other neuroendocrine systems regulating the thyroid, metabolic, and stress axes and their physiological responses. Weakly estrogenic and anti-androgenic pollutants such as bisphenol A, phthalates, phytochemicals, and the fungicide vinclozolin can lead to severe and widespread neuroendocrine disruptions in discrete brain regions, including the hippocampus, amygdala, and hypothalamus, resulting in behavioral changes in a wide range of species. Behavioral features that have been shown to be affected by one or more these chemicals include cognitive deficits, heightened anxiety or anxiety-like, sociosexual, locomotor, and appetitive behaviors. Neuroactive pharmaceuticals are now widely detected in aquatic environments and water supplies through the release of wastewater treatment plant effluents. The antidepressant fluoxetine is one such pharmaceutical neuroendocrine disruptor. Fluoxetine is a selective serotonin reuptake inhibitor that can affect multiple neuroendocrine pathways and behavioral circuits, including disruptive effects on reproduction and feeding in fish. There is growing evidence for the association between environmental contaminant exposures and diseases with strong neuroendocrine components, for example decreased fecundity, neurodegeneration, and cardiac disease. It is critical to consider the timing of exposures of neuroendocrine disruptors because embryonic stages of central nervous system development are exquisitely sensitive to adverse effects. There is also evidence for epigenetic and transgenerational neuroendocrine disrupting effects of some pollutants. We must now consider the impacts of neuroendocrine disruptors on reproduction, development, growth and behaviors, and the population consequences for evolutionary change in an increasingly contaminated world. This review examines the evidence to date that various so-called neuroendocrine disruptors can induce such effects often at environmentally-relevant concentrations.

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Section: Legacy Pesticides As Neuroendocrine Disruptorsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Current concepts in neuroendocrine disruption

León-Olea

Martyniuk

Orlando

et al. 2014

General and Comparative Endocrinology

126

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“…Hormones are mostly catabolised in the liver. Consequently, EDCs can participate in most aforementioned pathways thereby changing hormone synthesis patterns, mimicing hormone function or blocking it by occupying the receptor site, modulating the number of the receptors and their affinities for specific molecules and altering hormone clearance (Gore et al, 2006;Gore, 2007;Gore, 2008). Sex hormones synthesis is regulated by the hypothalamic-pituitary-gonadal axis.…”

Section: Pesticides As Endocrine Disrupting Chemicals (Edc)mentioning

confidence: 99%

Pesticide Exposure and Health Related Issues in Male and Female Reproductive System

Sifakis¹,

Mparmpas²,

Tsatsakis³

2011

Pesticides - Formulations, Effects, Fate

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“…The physiological features of brain sexual differentiation make it potentially susceptible to the endocrine-disrupting effects of different man-made and naturally occurring compounds with sex steroid agonistic or antagonistic activities (3,7). However, the environmental and (eventual) clinical relevance of exposures to such endocrine-disrupting compounds (EDCs) is yet to be established fully (8).…”

mentioning

confidence: 99%

“…Although such a possibility has been recently put forward (7,11), the mechanisms and targets for such a disruption of the reproductive neuroendocrine systems remain to date ill defined and warrant further investigation.…”

mentioning

confidence: 99%

Persistent Impairment of Hypothalamic KiSS-1 System after Exposures to Estrogenic Compounds at Critical Periods of Brain Sex Differentiation

et al. 2008

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Attainment of reproductive capacity at puberty relies on a complex series of maturational events that include sexual differentiation of the brain; a hormonally driven phenomenon that takes place at early stages of development (critical period). Alterations of sex steroid milieu during such critical period disrupt pubertal maturation and gonadotropic function later in life, through mechanisms that remain partially unknown. Kisspeptins, products of the KiSS-1 gene acting via G protein-coupled receptor 54, have recently emerged as essential gatekeepers of puberty onset and reproductive function. By using rat models of neonatal administration of estrogenic compounds, we provide herein compelling evidence for the functional impairment of the hypothalamic KiSS-1 system at the time preceding puberty after early inappropriate exposures during brain sex differentiation. Neonatal injection of estradiol benzoate to male and female rats resulted in a dose-dependent decrease in hypothalamic KiSS-1 mRNA levels at the prepubertal stage, linked to lowering of serum LH concentrations. Yet, despite persistently decreased basal gonadotropin levels in estrogenized animals, intracerebral injection of kisspeptin evoked potent LH and FSH secretory responses, similar in magnitude to those of control animals. Estrogenized rats also showed defective levels of hypothalamic KiSS-1 mRNA and circulating gonadotropins in response to gonadectomy, whereas exogenous kisspeptin was capable to enhance further LH and FSH secretion in this model. Finally, protocols of neonatal exposure to high doses of an environmentally relevant estrogen, bisphenol-A, mimicked the effects of estradiol benzoate in terms of hypothalamic expression of KiSS-1 gene at the prepubertal period. Altogether, our data document the sensitivity of the hypothalamic KiSS-1 system to alterations in sex steroid milieu during critical periods of brain sex differentiation, and suggest that lowering of endogenous kisspeptin tone induced by early exposures to xeno-estrogens might be mechanistically relevant for disruption of gonadotropin secretion and puberty onset later in life.

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Neuroendocrine systems as targets for environmental endocrine-disrupting chemicals

Cited by 29 publications

References 18 publications

Current concepts in neuroendocrine disruption

Current concepts in neuroendocrine disruption

Pesticide Exposure and Health Related Issues in Male and Female Reproductive System

Persistent Impairment of Hypothalamic KiSS-1 System after Exposures to Estrogenic Compounds at Critical Periods of Brain Sex Differentiation

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