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ToxSci Advance Access published online on October 27, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfi015
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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Received September 27, 2004
Accepted October 20, 2004

Endocrine Toxicology

Novel Progestogenic Activity of Environmental Endocrine Disruptors in the Up-Regulation of Calbindin-D9k in an Immature Mouse Model

Yong-Woo Jung 1, Eui-Ju Hong 1, Kyung-Chul Choi 2, and Eui-Bae Jeung 1*

1 Laboratory of Veterinary Biochemistry and Molecular Biology, College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, 361-763 Republic of Korea
2 Department of Obstetrics and Gynecology, British Columbia Children's and Women's Hospital, British Columbia Research Institute for Children's and Women's Health, University of British Columbia, Vancouver, BC, V6H 3V5 Canada

* To whom correspondence should be addressed.
Eui-Bae Jeung, E-mail: ebjeung{at}chungbuk.ac.kr


  Abstract

Endocrine disruption is a major global health concern in industrialized world. The induction of uterine Calbindin-D9k (CaBP-9k), which belongs to a large family of intracellular calcium binding proteins, was used to assess the exposure of endocrine disruptors (EDs) in an immature mouse model. Sex steroid hormones have been demonstrated to regulate uterine CaBP-9k expression in the uterus of rats and mice. In particular, the mouse CaBP-9k gene was predominantly regulated by progesterone (P4), whereas rat CaBP-9k was mainly induced by 17beta-estradiol (E2) in the uterus. In the present study, immature (14-day-old) female mice were injected with 4-tert-octylphenol (OP), nonylphenol (NP), bisphenol A (BPA), E2 or P4 to determine their effects on uterine CaBP-9k mRNA and protein expression. In addition, to specify estrogenic or progestogenic activity of EDs in the regulation of CaBP-9k, the mice were co-treated with ICI 182,780, an estrogen receptor (ER) antagonist or RU486, a progesterone receptor (PR) antagonist,. Treatments with OP, NP or BPA resulted in an increased CaBP-9k mRNA and protein in the uterus of immature mice in dose- and time-dependent manner. The EDs-induced expression of CaBP-9k mRNA and protein was reversed or abolished by pre-treatment with RU486 or ICI 182,780, suggesting that these synthetic chemicals may have both progestogenic and estrogenic properties by acting through PR or ER in the induction of uterine CaBP-9k mRNA and protein in this model. These results describe a novel in vivo model for detection of both estrogenic and progestogenic activities of EDs in the induction of CaBP-9k mRNA and protein in the uterus of immature mice.

Keywords: Calbindin-D9k; endocrine disruptor; estradiol; progesterone.
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