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Molecular mechanism(s) of endocrine‐disrupting chemicals and their potent oestrogenicity in diverse cells and tissues that express oestrogen receptors
Authors:Hye‐Rim Lee  Eui‐Bae Jeung  Myung‐Haing Cho  Tae‐Hee Kim  Peter C K Leung  Kyung‐Chul Choi
Institution:1. Laboratory of Veterinary Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, , Cheongju, Chungbuk, Korea;2. Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, , Seoul, Korea;3. Advanced Institute of Convergence Technology, Seoul National University, Suwon, , Korea;4. Department of Obstetrics and Gynecology, College of Medicine, Soonchunhyang University, , Bucheon, Korea;5. Department of Obstetrics and Gynecology, Child and Family Research Institute, Faculty of Medicine, University of British Columbia, , Vancouver, British Columbia, Canada
Abstract:Endocrine‐disrupting chemicals (EDCs) are natural or synthetic compounds present in the environment which can interfere with hormone synthesis and normal physiological functions of male and female reproductive organs. Most EDCs tend to bind to steroid hormone receptors including the oestrogen receptor (ER), progesterone receptor (PR) and androgen receptor (AR). As EDCs disrupt the actions of endogenous hormones, they may induce abnormal reproduction, stimulation of cancer growth, dysfunction of neuronal and immune system. Although EDCs represent a significant public health concern, there are no standard methods to determine effect of EDCs on human beings. The mechanisms underlying adverse actions of EDC exposure are not clearly understood. In this review, we highlighted the toxicology of EDCs and its effect on human health, including reproductive development in males and females as shown in in vitro and in vivo models. In addition, this review brings attention to the toxicity of EDCs via interaction of genomic and non‐genomic signalling pathways through hormone receptors.
Keywords:endocrine‐disrupting chemicals  oestrogen receptor  oestrogenicity
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