Comparative Overview of the Mechanisms of Action of Hormones and Endocrine Disruptor Compounds

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Endocrine Disruptor Compounds (EDCs) are synthetic or natural molecules in the environment that promote adverse modifications of endogenous hormone regulation in humans and/or in wildlife animals. In the present paper, we review the potential mechanisms of EDCs and point out the similarities and differences between EDCs and hormones. There was only one mechanism, out of nine identified, in which EDCs acted like hormones (i.e., binding and stimulated hormone receptor activity). In the other eight identified mechanisms of action, EDCs exerted their effects either by affecting endogenous hormone concentration, or its availability, or by modifying hormone receptor turn over. This overview is intended to classify the various EDC mechanisms of action in order to better appreciate when in vitro tests would be valid to assess their risks towards humans and wildlife.

Related collections

Most cited references 62

Record: found
Abstract: found
Article: not found

Fate of endocrine-disruptor, pharmaceutical, and personal care product chemicals during simulated drinking water treatment processes.

Paul Westerhoff, Yeomin Yoon, Shane Snyder … (2005)

The potential occurrence of endocrine-disrupting compounds (EDCs) as well as pharmaceuticals and personal care products (PPCPs) in drinking water supplies raises concern over the removal of these compounds by common drinking water treatment processes. Three drinking water supplies were spiked with 10 to 250 ng/L of 62 different EDC/ PPCPs; one model water containing an NOM isolate was spiked with 49 different EDC/PPCPs. Compounds were detected by LC/MS/MS or GC/MS/MS. These test waters were subjected to bench-scale experimentation to simulate individual treatment processes in a water treatment plant (WTP). Aluminum sulfate and ferric chloride coagulants or chemical lime softening removed some polyaromatic hydrocarbons (PAHs) but removed 98% of GC/ MS/MS compounds (more volatile) and 10% to >95% of LC/ MS/MS compounds (more polar); higher PAC dosages improved EDC/PPCP removal. EDC/PPCP percentage removal was independent of the initial compound concentration. Octanol-water partition coefficients served as a reasonable indicator of compound removal under controlled PAC test conditions, except for EDC/PPCPs that were protonated or deprotonated at the test pH and some that contained heterocyclic or aromatic nitrogen. Separate chlorine or ozone experiments decreased the EDC/PPCP initial concentration by 90%; EDC/PPCPs were likely transformed to oxidation byproducts. Ozone oxidized steroids containing phenolic moieties (estradiol, ethynylestradiol, or estrone) more efficiently than those without aromatic or phenolic moieties (androstenedione, progesterone, and testosterone). EDC/PPCP reactivity with oxidants were separated into three general groups: (1) compounds easily oxidized (>80% reacted) by chlorine are always oxidized at least as efficiently by ozone; (2) 6 of the -60 compounds (TCEP, BHC, chlordane, dieldrin, heptachlor epoxide, musk ketone) were poorly oxidized (<20% reacted) by chlorine or ozone; (3) compounds (24 of 60) reacting preferentially (higher removals) with ozone rather than chlorine. Conventional treatment (coagulation plus chlorination) would have low removal of many EDC/PPCPs, while addition of PAC and/or ozone could substantially improve their removals. Existing strategies that predict relative removals of herbicides, pesticides, and other organic pollutants by activated carbon or oxidation can be directly applied for the removal of many EDC/PPCPs, but these strategies need to be modified to account for charged (protonated bases or deprotonated acids) and aliphatic species. Some compounds (e.g., DEET, ibuprofen, gemfibrozil) had low removals unless ozonation was used. Other compounds had low removals by all the WTP processes considered (atrazine, iopromide, meprobamate, TCEP), and removal processes capable of removing these types of compounds should be investigated.

0 comments Cited 195 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Epigenetics as a mechanism linking developmental exposures to long-term toxicity

Z Herceg, J. Beckers, J. Chen … (2018)

A variety of experimental and epidemiological studies lend support to the Developmental Origin of Health and Disease (DOHaD) concept. Yet, the actual mechanisms accounting for mid- and long-term effects of early-life exposures remain unclear. Epigenetic alterations such as changes in DNA methylation, histone modifications and the expression of certain RNAs have been suggested as possible mediators of long-term health effects of environmental stressors. This report captures discussions and conclusions debated during the last Prenatal Programming and Toxicity meeting held in Japan. Its first aim is to propose a number of criteria that are critical to support the primary contribution of epigenetics in DOHaD and intergenerational transmission of environmental stressors effects. The main criteria are the full characterization of the stressors, the actual window of exposure, the target tissue and function, the specificity of the epigenetic changes and the biological plausibility of the linkage between those changes and health outcomes. The second aim is to discuss long-term effects of a number of stressors such as smoking, air pollution and endocrine disruptors in order to identify the arguments supporting the involvement of an epigenetic mechanism. Based on the developed criteria, missing evidence and suggestions for future research will be identified. The third aim is to critically analyze the evidence supporting the involvement of epigenetic mechanisms in intergenerational and transgenerational effects of environmental exposure and to particularly discuss the role of placenta and sperm. While the article is not a systematic review and is not meant to be exhaustive, it critically assesses the contribution of epigenetics in the long-term effects of environmental exposures as well as provides insight for future research.

0 comments Cited 65 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Bisphenol A: an endocrine and metabolic disruptor.

Patrick Fénichel, Nicolas Chevalier, Françoise Brücker-Davis (2013)

Bisphenol A (BPA), initially designed, like diethylstilbestrol, as a synthetic estrogen, has been rapidly and widely used for its cross-linking properties in the manufacture of polycarbonate plastics and epoxy resins. Because of incomplete polymerization and degradation of the polymers by exposure to higher than usual temperatures, BPA leaches out from food and beverage containers, as well as from dental sealants. In humans, free active unconjugated BPA is metabolized by rapid glucurono- or sulfo-conjugation and eliminated via renal clearance. However, exposure to environmental nanomolar concentrations of BPA is ubiquitous and continuous via different routes: oral, air, skin. In rodents, fetal and perinatal exposure to such environmentally relevant doses of BPA has been shown to affect the brain, liver, gut, adipose tissue, endocrine pancreas, mammary gland and reproductive tract and function. Similar concentrations are also able in vitro to impact human malignant breast, prostate, male germ or adipocyte cell lines (with a promoting effect and by interfering with chemotherapy drugs), or to stimulate pancreatic β cell insulin secretion. High levels of BPA have recently been correlated with obesity, diabetes, cardiovascular diseases, polycystic ovarian disease or low sperm count. However, before the real impact of BPA on human health can be clearly assessed, prospective longitudinal epidemiological studies are needed as well as characterization of selective biomarkers to verify long-term exposure and selective imprinting.

0 comments Cited 57 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Toxics

Journal ID (iso-abbrev): Toxics

Journal ID (publisher-id): toxics

Title: Toxics

Publisher: MDPI

ISSN (Electronic): 2305-6304

Publication date (Electronic): 24 January 2019

Publication date Collection: March 2019

Volume: 7

Issue: 1

Electronic Location Identifier: 5

Affiliations

[1 ]CNRS, INRA, Physiologie de la Reproduction & des Comportements, 37380 Nouzilly, France; nguyenthimongdiep@ 123456qnu.edu.vn

[2 ]Faculty of Biology-Agricultural Engineering, Quy Nhon University, Binh Dinh 820000, Vietnam

Author notes

[* ]Correspondence: yves.combarnous@ 123456inra.fr

Author information

Yves Combarnous https://orcid.org/0000-0002-0574-2025

Thi Mong Diep Nguyen https://orcid.org/0000-0001-6534-9041

Article

Publisher ID: toxics-07-00005

DOI: 10.3390/toxics7010005

PMC ID: 6468742

PubMed ID: 30682876

SO-VID: bf81b389-fb7d-4ffe-811e-5395fbf5bade

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Comparative Overview of the Mechanisms of Action of Hormones and Endocrine Disruptor Compounds

Read this article at

Abstract

Related collections

Sex hormones and lung development

Most cited references 62

Fate of endocrine-disruptor, pharmaceutical, and personal care product chemicals during simulated drinking water treatment processes.

Epigenetics as a mechanism linking developmental exposures to long-term toxicity

Bisphenol A: an endocrine and metabolic disruptor.

Author and article information

Journal

Affiliations

Author notes

Author information

Article

History

Categories

Comments

Comment on this article

Similar content 300

Cited by 33

Most referenced authors 711