scholarly journals Expression of Estrogenic Response Genes in Black Mollies (Poecilia Sphenops) Exposed to Pyrogenic Hydrocarbon and Petroleum from Campeche Sound

2019 ◽  
Vol 39 (04) ◽  
Author(s):  
Maurilio Lara-Flores . ◽  
Jaime Rendon von Osten Sharma
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Endocrine Disruption ◽  
Endocrine Disrupting Compounds ◽  
Molecular Biomarker ◽  
Estrogenic Effects ◽  
Endocrine Disrupting ◽  
Poecilia Sphenops ◽  
Vitellogenin Genes

The estrogenic effects of endocrine disrupting compounds (EDC´s) in animals are not reversible and can reduce populations. Sensitive methods such Q-PCR have been used to determine changes in gene expression and thus predict the effects before they become irreversible. The present study was designed to detect the expression on the estrogen receptors and vitellogenin genes in the Black Mollies fish (Poecilia sphenops) exposed to pyrogenic hydrocarbon and petroleum from Campeche Sound. The results indicate that the expression of transcript of the estrogen receptor and vitellogenin indicates are potentially useful as molecular biomarker for detecting the presence of endocrine-disruption compounds in environment.

scholarly journals Symbiotic Gene Activation is Interrupted by Endocrine Disrupting Chemicals

2001 ◽  
Vol 1 ◽  
pp. 653-655 ◽  
Author(s):  
Jennifer E. Fox ◽  
Matthew E. Burow ◽  
John A. McLachlan
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Estrogen Receptors ◽  
Mammalian Cell Culture ◽  
Endocrine Disrupting Chemicals ◽  
Gene Activation ◽  
Symbiotic Gene ◽  
Endocrine Disrupting ◽  
Plant Chemicals ◽  
By Products

Endocrine disrupting chemicals (EDCs) include organochlorine pesticides, plastics manufacturing by-products, and certain herbicides[1]. These chemicals have been shown to disrupt hormonal signaling in exposed wildlife, lab animals, and mammalian cell culture by binding to estrogen receptors (ER-α and ER-β) and affecting the expression of estrogen responsive genes[2,3]. Additionally, certain plant chemicals, termed phytoestrogens, are also able to bind to estrogen receptors and modulate gene expression, and as such also may be considered EDCs[4]. One example of phytoestrogen action is genistein, a phytochemical produced by soybeans, binding estrogen receptors, and changing expression of estrogen responsive genes which certain studies have linked to a lower incidence of hormonally related cancers in Japanese populations[5]. Why would plants make compounds that are able to act as estrogens in the human body? Obviously, soybeans do not intentionally produce phytoestrogens to prevent breast cancer in Japanese women.

scholarly journals Endocrine-Disrupting Chemicals: Associated Disorders and Mechanisms of Action

2012 ◽  
Vol 2012 ◽  
pp. 1-52 ◽  
Author(s):  
Sam De Coster ◽  
Nicolas van Larebeke
Keyword(s):  
Estrogen Receptors ◽  
Endocrine Disruptors ◽  
Endocrine Disruption ◽  
Cross Talk ◽  
Flame Retardants ◽  
Receptor Activation ◽  
Neuroendocrine Cells ◽  
Hair Dyes ◽  
The Metabolic Syndrome ◽  
Endocrine Disrupting

The incidence and/or prevalence of health problems associated with endocrine-disruption have increased. Many chemicals have endocrine-disrupting properties, including bisphenol A, some organochlorines, polybrominated flame retardants, perfluorinated substances, alkylphenols, phthalates, pesticides, polycyclic aromatic hydrocarbons, alkylphenols, solvents, and some household products including some cleaning products, air fresheners, hair dyes, cosmetics, and sunscreens. Even some metals were shown to have endocrine-disrupting properties. Many observations suggesting that endocrine disruptors do contribute to cancer, diabetes, obesity, the metabolic syndrome, and infertility are listed in this paper. An overview is presented of mechanisms contributing to endocrine disruption. Endocrine disruptors can act through classical nuclear receptors, but also through estrogen-related receptors, membrane-bound estrogen-receptors, and interaction with targets in the cytosol resulting in activation of the Src/Ras/Erk pathway or modulation of nitric oxide. In addition, changes in metabolism of endogenous hormones, cross-talk between genomic and nongenomic pathways, cross talk with estrogen receptors after binding on other receptors, interference with feedback regulation and neuroendocrine cells, changes in DNA methylation or histone modifications, and genomic instability by interference with the spindle figure can play a role. Also it was found that effects of receptor activation can differ in function of the ligand.

scholarly journals Hormone-Activated Estrogen Receptors in Annelid Invertebrates: Implications for Evolution and Endocrine Disruption

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1731-1738 ◽  
Author(s):  
June Keay ◽  
Joseph W. Thornton
Keyword(s):  
Estrogen Receptors ◽  
Endocrine Disruption ◽  
Endocrine Disrupting Chemicals ◽  
Estrogen Signaling ◽  
Estrogen Sensitivity ◽  
Endocrine Disrupting ◽  
Platynereis Dumerilii ◽  
Bilaterian Animal ◽  
Capitella Capitata ◽  
And Behavior

As the primary mediators of estrogen signaling in vertebrates, estrogen receptors (ERs) play crucial roles in reproduction, development, and behavior. They are also the major mediators of endocrine disruption by xenobiotic pollutants that mimic or block estrogen action. ERs that are sensitive to estrogen and endocrine disrupters have long been thought to be restricted to vertebrates: although there is evidence for estrogen signaling in invertebrates, the only ERs studied to date, from mollusks and cephalochordates, have been insensitive to estrogen and therefore incapable of mediating estrogen signaling or disruption. To determine whether estrogen sensitivity is ancestral or a unique characteristic of vertebrate ERs, we isolated and characterized ERs from two annelids, Platynereis dumerilii and Capitella capitata, because annelids are the sister phylum to mollusks and have been shown to produce and respond to estrogens. Functional assays show that annelid ERs specifically activate transcription in response to low estrogen concentrations and bind estrogen with high affinity. Furthermore, numerous known endocrine-disrupting chemicals activate or antagonize the annelid ER. This is the first report of a hormone-activated invertebrate ER. Our results indicate that estrogen signaling via the ER is as ancient as the ancestral bilaterian animal and corroborate the estrogen sensitivity of the ancestral steroid receptor. They suggest that the taxonomic scope of endocrine disruption by xenoestrogens may be very broad and reveal how functional diversity evolved in a gene family central to animal endocrinology.

scholarly journals Estradiol and the Developing Brain

2008 ◽  
Vol 88 (1) ◽  
pp. 91-134 ◽  
Author(s):  
MARGARET M. McCARTHY
Keyword(s):  
Gene Expression ◽  
Endocrine Disrupting Compounds ◽  
Developing Brain ◽  
Early Gene ◽  
Calcium Handling ◽  
Neuroprotective Effects ◽  
Regulate Gene Expression ◽  
Endocrine Disrupting ◽  
The Brain ◽  
Considerable Concern

Estradiol is the most potent and ubiquitous member of a class of steroid hormones called estrogens. Fetuses and newborns are exposed to estradiol derived from their mother, their own gonads, and synthesized locally in their brains. Receptors for estradiol are nuclear transcription factors that regulate gene expression but also have actions at the membrane, including activation of signal transduction pathways. The developing brain expresses high levels of receptors for estradiol. The actions of estradiol on developing brain are generally permanent and range from establishment of sex differences to pervasive trophic and neuroprotective effects. Cellular end points mediated by estradiol include the following: 1) apoptosis, with estradiol preventing it in some regions but promoting it in others; 2) synaptogenesis, again estradiol promotes in some regions and inhibits in others; and 3) morphometry of neurons and astrocytes. Estradiol also impacts cellular physiology by modulating calcium handling, immediate-early-gene expression, and kinase activity. The specific mechanisms of estradiol action permanently impacting the brain are regionally specific and often involve neuronal/glial cross-talk. The introduction of endocrine disrupting compounds into the environment that mimic or alter the actions of estradiol has generated considerable concern, and the developing brain is a particularly sensitive target. Prostaglandins, glutamate, GABA, granulin, and focal adhesion kinase are among the signaling molecules co-opted by estradiol to differentiate male from female brains, but much remains to be learned. Only by understanding completely the mechanisms and impact of estradiol action on the developing brain can we also understand when these processes go awry.

Abstract 617: Bisphenol A Inhibits GPR30-Mediated Dilation of Mesenteric Resistance Arteries

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sarah Lindsey ◽  
Melyssa Bratton ◽  
John A McLachlan
Keyword(s):  
Estrogen Receptor ◽  
Bisphenol A ◽  
Cardiovascular Effects ◽  
Mesenteric Arteries ◽  
The Novel ◽  
Resistance Arteries ◽  
Endocrine Disrupting Chemical ◽  
Downstream Signaling ◽  
Estrogenic Effects ◽  
Endocrine Disrupting

We previously showed that activation of the membrane estrogen receptor GPR30 decreases blood pressure in hypertensive ovariectomized mRen2.Lewis rats and acutely dilates mesenteric resistance arteries. These studies suggest that GPR30 plays a role in estrogen’s beneficial cardiovascular effects. Bisphenol A (BPA) is an endocrine-disrupting chemical found in most manufactured plastic products that also binds to GPR30 in the nanomolar range. Clinical studies show a significant correlation between elevated urinary BPA and increased diagnosis of cardiovascular diseases including hypertension. Therefore, we hypothesized that BPA may disrupt the vasodilatory effects mediated by the novel estrogen receptor GPR30. Second-order mesenteric arteries from 15 week-old Lewis females were denuded and mounted on a wire myograph. Arteries were preconstricted with 10 μM phenylephrine before assessing the response to increasing concentrations of the selective GPR30 agonist G-1 (0.001-3 μM). Pretreatment with 10 μM BPA significantly inhibited G-1-induced relaxation of denuded vessels (Figure, *P<0.01). In summary, BPA blocked the vasodilatory actions of G-1 in vascular smooth muscle, perhaps by competing for GPR30 and/or altering its downstream signaling. We conclude that human exposure to BPA may interfere with the protective estrogenic effects mediated by GPR30.

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