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Correlation between dioxin and endometriosis: an epigenetic route to unravel the pathogenesis of the disease.
Arch Gynecol Obstet 2015; 292(5):973-86AG

Abstract

INTRODUCTION

Environmental toxicants can act as endocrine disrupters on the female reproductive system. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is resistant to degradation and due to its lipophilic nature, accumulates in the fat tissue and in the food chain. Human and animal exposure to TCDD affects levels of the steroid receptors and steroid-responsive gene expression and has an impact on metabolism and serum transport of steroids. Gene expression is commonly altered in endometriosis and in the eutopic endometrium of women with the disease. Aberrantly expressed genes include those associated with the regulation of transcription, proliferation, sex steroid metabolism, apoptosis, cell cycle, the immune response and cell adhesion.

METHODS

In this paper, we review the evidence about TCDD's effect on eutopic and ectopic endometrium, in order to unravel the machinery behind the dysregulation of immune and hormonal homeostasis caused by this environmental toxicant.

CONCLUSION

The evidence collected in this review suggests that TCDD could modulate transcription at multiple levels, including the epigenetic level, and via microRNAs, thus disturbing the physiologic processes mediated through the aryl hydrocarbon receptor pathways. Exposure to TCDD also modulates the immune response by influencing the production and action of endometrial cytokines and chemokines, destroying mucosal immunity of the reproductive tract and re-directing the tissue distribution and behavior of leukocytes. Despite this large body of evidence, current human-based epidemiological studies on the association between TCDD and endometriosis remain controversial.

Authors+Show Affiliations

Department of Environmental Sciences, Safety, Territory, Food and Health, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Gynecology and Obstetrics, Münster University Hospital, 48149, Münster, Germany.Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Via C. Valeria 1, 98125, Messina, Italy. antlagana@unime.it.Department of Environmental Sciences, Safety, Territory, Food and Health, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Environmental Sciences, Safety, Territory, Food and Health, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Via C. Valeria 1, 98125, Messina, Italy.Department of Obstetrics and Gynecology, São Paulo University (USP), São Paulo, Brazil.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25920525

Citation

Sofo, Vincenza, et al. "Correlation Between Dioxin and Endometriosis: an Epigenetic Route to Unravel the Pathogenesis of the Disease." Archives of Gynecology and Obstetrics, vol. 292, no. 5, 2015, pp. 973-86.
Sofo V, Götte M, Laganà AS, et al. Correlation between dioxin and endometriosis: an epigenetic route to unravel the pathogenesis of the disease. Arch Gynecol Obstet. 2015;292(5):973-86.
Sofo, V., Götte, M., Laganà, A. S., Salmeri, F. M., Triolo, O., Sturlese, E., ... Abrão, M. S. (2015). Correlation between dioxin and endometriosis: an epigenetic route to unravel the pathogenesis of the disease. Archives of Gynecology and Obstetrics, 292(5), pp. 973-86. doi:10.1007/s00404-015-3739-5.
Sofo V, et al. Correlation Between Dioxin and Endometriosis: an Epigenetic Route to Unravel the Pathogenesis of the Disease. Arch Gynecol Obstet. 2015;292(5):973-86. PubMed PMID: 25920525.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Correlation between dioxin and endometriosis: an epigenetic route to unravel the pathogenesis of the disease. AU - Sofo,Vincenza, AU - Götte,Martin, AU - Laganà,Antonio Simone, AU - Salmeri,Francesca Maria, AU - Triolo,Onofrio, AU - Sturlese,Emanuele, AU - Retto,Giovanni, AU - Alfa,Maria, AU - Granese,Roberta, AU - Abrão,Mauricio Simões, Y1 - 2015/04/29/ PY - 2015/02/17/received PY - 2015/04/23/accepted PY - 2015/4/30/entrez PY - 2015/4/30/pubmed PY - 2016/1/9/medline KW - 2,3,7,8-Tetrachlorodibenzo-p-dioxin KW - Aryl hydrocarbon receptor KW - Endometriosis KW - Epigenetics KW - Sex hormone receptors SP - 973 EP - 86 JF - Archives of gynecology and obstetrics JO - Arch. Gynecol. Obstet. VL - 292 IS - 5 N2 - INTRODUCTION: Environmental toxicants can act as endocrine disrupters on the female reproductive system. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is resistant to degradation and due to its lipophilic nature, accumulates in the fat tissue and in the food chain. Human and animal exposure to TCDD affects levels of the steroid receptors and steroid-responsive gene expression and has an impact on metabolism and serum transport of steroids. Gene expression is commonly altered in endometriosis and in the eutopic endometrium of women with the disease. Aberrantly expressed genes include those associated with the regulation of transcription, proliferation, sex steroid metabolism, apoptosis, cell cycle, the immune response and cell adhesion. METHODS: In this paper, we review the evidence about TCDD's effect on eutopic and ectopic endometrium, in order to unravel the machinery behind the dysregulation of immune and hormonal homeostasis caused by this environmental toxicant. CONCLUSION: The evidence collected in this review suggests that TCDD could modulate transcription at multiple levels, including the epigenetic level, and via microRNAs, thus disturbing the physiologic processes mediated through the aryl hydrocarbon receptor pathways. Exposure to TCDD also modulates the immune response by influencing the production and action of endometrial cytokines and chemokines, destroying mucosal immunity of the reproductive tract and re-directing the tissue distribution and behavior of leukocytes. Despite this large body of evidence, current human-based epidemiological studies on the association between TCDD and endometriosis remain controversial. SN - 1432-0711 UR - https://www.unboundmedicine.com/medline/citation/25920525/full_citation L2 - https://dx.doi.org/10.1007/s00404-015-3739-5 DB - PRIME DP - Unbound Medicine ER -