Gene-environment interactions in male reproductive health: Special reference to the aryl hydrocarbon receptor signaling pathway.
(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:
https://lup.lub.lu.se/record/4223005
- author
- Brokken, Leon LU and Giwercman, Yvonne LU
- organization
- publishing date
- 2014
- 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
- pmid:24369137
- 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
- 2016-04-01 09:59:33
- date last changed
- 2022-02-02 05:21:16
@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 = {{https://lup.lub.lu.se/search/files/1456305/4437288}},
doi = {{10.4103/1008-682X.122193}},
volume = {{16}},
year = {{2014}},
}