Octylphenol does not mimic diethylstilbestrol-induced oestrogen receptor-alpha expression in the newborn mouse uterine epithelium after prenatal exposure

Citation
M. Nielsen et al., Octylphenol does not mimic diethylstilbestrol-induced oestrogen receptor-alpha expression in the newborn mouse uterine epithelium after prenatal exposure, J ENDOCR, 167(1), 2000, pp. 29-37
Citations number
59
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF ENDOCRINOLOGY
ISSN journal
00220795 → ACNP
Volume
167
Issue
1
Year of publication
2000
Pages
29 - 37
Database
ISI
SICI code
0022-0795(200010)167:1<29:ODNMDO>2.0.ZU;2-M
Abstract
This study examined whether the endocrine disrupter octylphenol (OP) mimics the synthetic oestrogen diethylstilbestrol (DES) in ability to induce oest rogen receptor-alpha (ER-alpha) expression in the newborn mouse uterine epi thelium after prenatal exposure. Pregnant mice were given daily s.c. inject ions with DES (10 or 100 mug DES/kg maternal wt) or OP (100 or 250 mg/kg ma ternal wt) or with vehicle alone from day 11.5 to 16.5 of pregnancy. ER-alp ha expression was evaluated on histological sections by detecting ER-alpha mRNA with the in situ hybridization technique and ER-alpha protein using im munohistochemistry. The immunostaining was quantitated using a microspectro photometer. Oestrogen-like activity of the DES and OP batches used for in v ivo exposure was confirmed in an in vitro assay based on transient gene exp ression of an oestrogen-dependent reporter plasmid. In mice exposed prenata lly to vehicle alone, the uterine epithelium did not express either ER-alph a mRNA or protein, while both were highly expressed in the stroma. Exposure to either DES dose induced the expression of both ER-alpha mRNA and protei n in the epithelium, whereas it was unchanged in the stroma. In contrast, n either OP dose induced the expression of ER-alpha mRNA or protein in the ep ithelium and expression was unchanged in the stroma. Our data stress the im portance of in vivo studies when investigating endocrine disrupters.