Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction
- PMID: 15798013
- DOI: 10.1530/rep.1.00294
Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction
Abstract
The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlor-odibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.
Similar articles
-
Modulation of oestrogen receptor signalling by association with the activated dioxin receptor.Nature. 2003 May 29;423(6939):545-50. doi: 10.1038/nature01606. Nature. 2003. PMID: 12774124
-
Influence of aryl hydrocarbon- (Ah) receptor and genotoxins on DNA repair gene expression and cell survival of mouse hepatoma cells.Toxicology. 2009 May 17;259(3):91-6. doi: 10.1016/j.tox.2009.02.006. Epub 2009 Feb 28. Toxicology. 2009. PMID: 19428948
-
Intrinsic function of the aryl hydrocarbon (dioxin) receptor as a key factor in female reproduction.Mol Cell Biol. 2005 Nov;25(22):10040-51. doi: 10.1128/MCB.25.22.10040-10051.2005. Mol Cell Biol. 2005. PMID: 16260617 Free PMC article.
-
Dioxin toxicity, aryl hydrocarbon receptor signaling, and apoptosis-persistent pollutants affect programmed cell death.Crit Rev Toxicol. 2011 Apr;41(4):292-320. doi: 10.3109/10408444.2010.524635. Epub 2011 Feb 17. Crit Rev Toxicol. 2011. PMID: 21323611 Review.
-
Carcinogenic risks of dioxin: mechanistic considerations.Regul Toxicol Pharmacol. 2005 Oct;43(1):19-34. doi: 10.1016/j.yrtph.2005.05.008. Regul Toxicol Pharmacol. 2005. PMID: 16054739 Review.
Cited by
-
Assessment and molecular actions of endocrine-disrupting chemicals that interfere with estrogen receptor pathways.Int J Endocrinol. 2013;2013:501851. doi: 10.1155/2013/501851. Epub 2013 May 2. Int J Endocrinol. 2013. PMID: 23737774 Free PMC article.
-
Effects of Low-Dose Developmental Bisphenol A Exposure on Metabolic Parameters and Gene Expression in Male and Female Fischer 344 Rat Offspring.Environ Health Perspect. 2017 Jun 28;125(6):067018. doi: 10.1289/EHP505. Environ Health Perspect. 2017. PMID: 28657538 Free PMC article.
-
Temporal and anatomical sensitivities to the aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin leading to premature acyclicity with age in rats.Int J Androl. 2010 Apr;33(2):405-12. doi: 10.1111/j.1365-2605.2009.01031.x. Epub 2010 Jan 4. Int J Androl. 2010. PMID: 20059580 Free PMC article.
-
High levels of follicular fluid testosterone could impair oocyte developmental competency via affecting aryl hydrocarbon receptor pathway in PCOS patients.BMC Mol Cell Biol. 2022 Nov 11;23(1):47. doi: 10.1186/s12860-022-00449-y. BMC Mol Cell Biol. 2022. PMID: 36368943 Free PMC article.
-
Genomewide analysis of aryl hydrocarbon receptor binding targets reveals an extensive array of gene clusters that control morphogenetic and developmental programs.Environ Health Perspect. 2009 Jul;117(7):1139-46. doi: 10.1289/ehp.0800485. Epub 2009 Mar 24. Environ Health Perspect. 2009. PMID: 19654925 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources