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Abstract

Abstract

Aryl Hydrocarbon Receptor (AhR) ligands are ubiquitous endocrine disrupting chemicals (EDCs) used in consumer products, diet, air and water. These chemicals are reproductive toxicants which promote tumor formation in some reproductive model systems but human data are limited. The occurrence of reproductive tumors was exponentially grown during the last three decades especially in Tehran but the underlying risk factors remained unclear. A cross-sectional case control study was conducted on the tissue and serological levels of AhR, sex steroid receptors and 120 lifestyle in relation to exposure to EDCs in 500 premenopausal women with history of endometriosis, uterine leiomyoma, breast fibroadenoma and breast cancer from 2007–2011.Differential levels of AhR, ER, PR ,AR, were determined in mentioned female reproductive tumors . Their association with lifestyle factors was also examined in different female tumors. Logistic regression was used to estimate odds ratios (ORs) and 95 percent confidence intervals (CIs), adjusting for potential risk factors. AhR overexpression in epithelial cells of premenopausal patients emphasized the susceptibility of these cells to environmental induced reproductive disorders. Living near PAHs producing factories, consumption of animal fat, abnormal weight gain, long term (>5yrs) OCP consumption, smoking, severe stress, hormonal deregulations and exposure to other sources of xenoestrogens were correlated with an increased risk of reproductive tumors which were correlated with elevated tissue levels of AhR. Adiposity and abnormal weight gain after 18 years were considered as two major background factors, which may contribute to the levels of endogenous estrogens. It seems that AhR overexpression is affected by exposure to xenoestrogens and by adiposity. Long term exposure to EDCs can increase the tissue levels of AhR and deregulate the expression pattern of sex steroid receptors and other genes in target tissues.

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/content/papers/10.5339/qproc.2012.mutagens.3.12
2012-03-01
2019-10-17
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http://instance.metastore.ingenta.com/content/papers/10.5339/qproc.2012.mutagens.3.12
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  • Received: 07 May 2012
  • Accepted: 07 May 2012
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