Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway
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...
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Format: | Article |
Language: | English |
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Wolters Kluwer Medknow Publications
2014-02-01
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Series: | Asian Journal of Andrology |
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Online Access: | http://www.ajandrology.com/article.asp?issn=1008-682X;year=2014;volume=16;issue=1;spage=89;epage=96;aulast=Brokken |
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author | Leon J S Brokken Yvonne Lundberg Giwercman |
author_facet | Leon J S Brokken Yvonne Lundberg Giwercman |
author_sort | Leon J S Brokken |
collection | DOAJ |
description | 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. |
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format | Article |
id | doaj.art-d849b90bee5240279307bc99da36e45a |
institution | Directory Open Access Journal |
issn | 1008-682X 1745-7262 |
language | English |
last_indexed | 2024-12-11T09:31:13Z |
publishDate | 2014-02-01 |
publisher | Wolters Kluwer Medknow Publications |
record_format | Article |
series | Asian Journal of Andrology |
spelling | doaj.art-d849b90bee5240279307bc99da36e45a2022-12-22T01:13:01ZengWolters Kluwer Medknow PublicationsAsian Journal of Andrology1008-682X1745-72622014-02-01161899610.4103/1008-682X.122193Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathwayLeon J S Brokken0Yvonne Lundberg Giwercman1Department of Clinical Sciences, Molecular Genetic Reproductive Medicine, Lund University, Malmö, SwedenDepartment of Clinical Sciences, Molecular Genetic Reproductive Medicine, Lund University, Malmö, SwedenOver 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.http://www.ajandrology.com/article.asp?issn=1008-682X;year=2014;volume=16;issue=1;spage=89;epage=96;aulast=Brokkenandrogen receptor; aryl hydrocarbon receptor; endocrine disrupter |
spellingShingle | Leon J S Brokken Yvonne Lundberg Giwercman Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway Asian Journal of Andrology androgen receptor; aryl hydrocarbon receptor; endocrine disrupter |
title | Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway |
title_full | Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway |
title_fullStr | Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway |
title_full_unstemmed | Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway |
title_short | Gene-environment interactions in male reproductive health: special reference to the aryl hydrocarbon receptor signaling pathway |
title_sort | gene environment interactions in male reproductive health special reference to the aryl hydrocarbon receptor signaling pathway |
topic | androgen receptor; aryl hydrocarbon receptor; endocrine disrupter |
url | http://www.ajandrology.com/article.asp?issn=1008-682X;year=2014;volume=16;issue=1;spage=89;epage=96;aulast=Brokken |
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