Junzo Yonemoto* and Hideko Sone*

* National Institute for Environmental Studies

+ Correspondence should be addressed to Junzo Yonemoto:
(16-2, Onogawa, Tsukuba, Ibaraki 305-0053 Japan)

Abstract

In this study, the responsiveness to TCDD in cell lines from sex hormone-dependent tissues and rat's liver were investigated, using CYP1A1 as a marker, to elucidate the mechanisms involved in the interaction between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and sex hormones. In endometrial carcinoma cell lines, RL95-2 and KLE, estrogen receptor [alpha] (ER[alpha]) plays a very important role in the positive regulation of genes associated with the arylhydrocarbon receptor (AhR) gene battery and is mainly responsible for the differential responses of the two cell lines to TCDD. In rat's liver, estrogen enhanced the TCDD induced CYP1A1 expression in vivo. On the other hand, the potent antiandrogenic effect of TCDD and a bilateral transcriptional interference between testosterone and TCDD-induced signal transduction pathways were observed in LNCaP prostate cancer cells.

Key words: dioxin, estrogen receptor, CYP1A1, testosterone