Endocrine Disruptors in Endometriosis
Keywords:
endometriosis, endocrine disruptors, infertility, bisphenol-A, phthalate, PCBs, TCDD
Abstract
Endometriosis is an estrogen-dependent disease, which involves the growth of endometrial tissue outside the uterine cavity, commonly in the pelvic region. The etiology of the disease is unclear, but multiple factors may contribute to its prognosis. Toxicological studies indicate that many chemicals are able to interfere with endocrine homeostasis, called endocrine disrupting chemicals (EDC) like Bisphenol A, Phtalate, Polychlorinated Biphenyls and Dioxins. As well documented, endometriosis is an estrogen-dependent disease; therefore, environmental toxicants that either mimic estrogen or enhance estrogenic exposure in the endometrium are thought to increase the risk of endometriosis. The purpose of this mini-review is to provide an overview of epidemiological studies, which have evaluated the relationship between endometriosis and exposure to endocrine disruptors.
Downloads
- Article PDF
- TEI XML Kaleidoscope (download in zip)* (Beta by AI)
- Lens* NISO JATS XML (Beta by AI)
- HTML Kaleidoscope* (Beta by AI)
- DBK XML Kaleidoscope (download in zip)* (Beta by AI)
- LaTeX pdf Kaleidoscope* (Beta by AI)
- EPUB Kaleidoscope* (Beta by AI)
- MD Kaleidoscope* (Beta by AI)
- FO Kaleidoscope* (Beta by AI)
- BIB Kaleidoscope* (Beta by AI)
- LaTeX Kaleidoscope* (Beta by AI)
How to Cite
References
S. Ahmed (2005) Protein kinase Cθ activity is involved in the 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐induced signal transduction pathway leading to apoptosis in L‐MAT, a human lymphoblastic T‐cell line. 272(4), 903-915.
O. Albert (2013) Jégou, B., 2013 A critical assessment of the endocrine susceptibility of the human testis to phthalates from fetal life to adulthood. 20(0), 1-19.
E. Attar, S. Bulun (2006) Aromatase and other steroidogenic genes in endometriosis: translational aspects. 12(1), 49-56. https://doi.org/10.1093/humupd/dmi034
R. Barbieri (1990) Etiology and epidemiology of endometriosis. 162(2), 565-567.
M. Van den Berg (2006) et al., 2006 The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds. 93(2), 223-241.
P. Bigey (2000) et al., 2000 Transcriptional regulation of the human DNA Methyltransferase (dnmt1) gene. 242(1-2), 407-418.
F. Bischoff (2004) Genetic Basis of Endometriosis. 299, 284-299.
Buck Louis, G. (2013) et al., 2013 Bisphenol A and phthalates and endometriosis: the Endometriosis: Natural History, Diagnosis and Outcomes Study. 100(1), 1-2.
K. Burns (2012) et al., 2012 Role of estrogen receptor signaling required for endometriosis-like lesion establishment in a mouse model. 153(8), 3960-3971.
D. Caserta (2008) et al., 2008 Impact of endocrine disruptor chemicals in gynaecology. 14(1), 59-72. https://doi.org/10.1093/humupd/dmm025
D. Caserta (2013) et al., 2013 The influence of endocrine disruptors in a selected population of infertile women. 29(5), 444-447.
W. Chang, J. Hung (2012) Functional role of post-translational modifications of Sp1 in tumorigenesis. 19, 94.
L. Cobellis (2009) et al., 2009 Measurement of bisphenol A and bisphenol B levels in human blood sera from healthy and endometriotic women. 23(11), 1186-1190.
W. Foster, S. Maharaj-Briceño (2010) Dioxin-Induced Changes in Epididymal Sperm Count and Spermatogenesis. 118(4), 458-464.
S.-W Guo (2009) Epigenetics of endometriosis. 15(10), 587-607. https://doi.org/10.1093/molehr/gap064
J. Halme (1984) et al., 1984 Retrograde menstruation in healthy women and in patients with endometriosis. 64(2), 151-154.
S. Han (2015) et al., 2015 Estrogen Receptor β Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis. 163(4), 960-974. https://doi.org/10.1016/j.cell.2015.10.034
F. Howard (1993) The Role of Laparoscopy in Chronic Pelvic Pain: Promise and Pitfalls. 48(6), 357-387.
C. Ishida (2003) et al., 2003 Genomic organization and promoter analysis of the Dnmt3b gene. 310, 151-159.
H. Itoh (2007) et al., 2007 Urinary bisphenol-A concentration in infertile Japanese women and its association with endometriosis: A cross-sectional study. 12(6), 258-264.
M. Kogevinas Human health effects of dioxins: cancer, reproductive and endocrine system effects. 7(3), 331-339.
Y. Lee (2011) et al., 2011 2,3,7,8-Tetrachlorodibenzo-pdioxin-induced MUC5AC expression: aryl hydrocarbon receptor-independent/EGFR/ERK/p38- dependent SP1-based transcription. 45(2), 270-276.
M. Levin (2005) et al., 2005 Non-coplanar PCB-mediated modulation of human leukocyte phagocytosis: a new mechanism for immunotoxicity Journal of toxicology and environmental health. 68(22).
A. Mantovani (2006) Risk assessment of endocrine disrupters: the role of toxicological studies. 1076, 239-252.
J. Mimura (2003) Functional role of AhR in the expression of toxic effects by TCDD. 1619(3), 263-268.
E. Oh (2005) et al., 2005 Evaluation of immuno- and reproductive toxicities and association between immunotoxicological and genotoxicological parameters in waste incineration workers. 210(1), 65-80. https://doi.org/10.1016/j.tox.2005.01.008
N. Puebla-Osorio (2004) et al., 2004 2,3,7,8- Tetrachlorodibenzo-p-dioxin elicits aryl hydrocarbon receptor-mediated apoptosis in the avian DT40 pre- B-cell line through activation of caspases 9 and 3 Comparative biochemistry and physiology. 138(4), 461-468.
J. Rawson (1991) Prevalence of endometriosis in asymptomatic women. 36(7), 513-515.
A. Schecter (2006) et al., 2006 Dioxins: an overview. 101(3), 419-428.
Y. Shimizu (2000) et al., 2000 Benzo[a]pyrene carcinogenicity is lost in mice lacking the aryl hydrocarbon receptor. 97(2), 779-782.
P. Simsa (2010) Increased exposure to dioxin-like compounds is associated with endometriosis in a case-control study in women. 20, 681-688.
S. Singh (2012) Epigenetic Effects of Environmental Chemicals Bisphenol A and Phthalates. 13(8), 0143-1015.
M. Ulukus, H. Cakmak (2006) The Role of Endometrium in Endometriosis. 13(7), 467-476.
K. Upson (2013) Phthalates and risk of endometriosis. 1-7.
Y. Zhao (2015) Dual suppression of estrogenic and inflammatory activities for targeting of endometriosis. 7(271), 271ra9.
Published
2016-08-15
Issue
Section
License
Copyright (c) 2016 Authors and Global Journals Private Limited

This work is licensed under a Creative Commons Attribution 4.0 International License.