Advanced

Gene-environment interactions in male reproductive health: Special reference to the aryl hydrocarbon receptor signaling pathway.

Brokken, Leon LU and Giwercman, Yvonne LU (2014) In Asian Journal of Andrology 16(1). p.89-96
Abstract
Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action, biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid... (More)
Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action, biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid pathways, in which the EDCs may act directly as agonists or antagonists, or indirectly via other nuclear receptors. Dioxins and dioxin-like EDCs exert their biological and toxicological actions through activation of the aryl hydrocarbon-receptor, which besides inducing transcription of detoxifying enzymes also regulates transcriptional activity of other nuclear receptors. There is increasing evidence that genetic predispositions may modify the susceptibility to adverse effects of toxic chemicals. In this review, potential consequences of hereditary predisposition and EDCs are discussed, with a special focus on the currently available publications on interactions between dioxin and androgen signaling. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Asian Journal of Andrology
volume
16
issue
1
pages
89 - 96
publisher
Nature Publishing Group
external identifiers
  • wos:000329409700011
  • pmid:24369137
  • scopus:84891904731
ISSN
1008-682X
DOI
10.4103/1008-682X.122193
language
English
LU publication?
yes
id
70b6c5c5-dd05-4bf3-a20a-05df4af003f4 (old id 4223005)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24369137?dopt=Abstract
date added to LUP
2014-01-06 13:29:53
date last changed
2017-11-19 03:03:25
@article{70b6c5c5-dd05-4bf3-a20a-05df4af003f4,
  abstract     = {Over the last few decades, there have been numerous reports of adverse effects on the reproductive health of wildlife and laboratory animals caused by exposure to endocrine disrupting chemicals (EDCs). The increasing trends in human male reproductive disorders and the mounting evidence for causative environmental factors have therefore sparked growing interest in the health threat posed to humans by EDCs, which are substances in our food, environment and consumer items that interfere with hormone action, biosynthesis or metabolism, resulting in disrupted tissue homeostasis or reproductive function. The mechanisms of EDCs involve a wide array of actions and pathways. Examples include the estrogenic, androgenic, thyroid and retinoid pathways, in which the EDCs may act directly as agonists or antagonists, or indirectly via other nuclear receptors. Dioxins and dioxin-like EDCs exert their biological and toxicological actions through activation of the aryl hydrocarbon-receptor, which besides inducing transcription of detoxifying enzymes also regulates transcriptional activity of other nuclear receptors. There is increasing evidence that genetic predispositions may modify the susceptibility to adverse effects of toxic chemicals. In this review, potential consequences of hereditary predisposition and EDCs are discussed, with a special focus on the currently available publications on interactions between dioxin and androgen signaling.},
  author       = {Brokken, Leon and Giwercman, Yvonne},
  issn         = {1008-682X},
  language     = {eng},
  number       = {1},
  pages        = {89--96},
  publisher    = {Nature Publishing Group},
  series       = {Asian Journal of Andrology},
  title        = {Gene-environment interactions in male reproductive health: Special reference to the aryl hydrocarbon receptor signaling pathway.},
  url          = {http://dx.doi.org/10.4103/1008-682X.122193},
  volume       = {16},
  year         = {2014},
}