Receptor-mediated effects of chlorinated hydrocarbons.

Abstract

This short review summarizes some recent findings on arylhydrocarbon (dioxin) receptor expression during early pregnancy in mammals. The arylhydrocarbon receptor is a ligand-activated transcription factor and was originally described as a mediator of the toxic effects of dioxins and other chlorinated hydrocarbons such as polychlorinated biphenyls. Orally administered polychlorinated biphenyls accumulate in uterine secretions, in the pre-implantation blastocyst, in the foetus and in the placenta. Coplanar polychlorinated biphenyls are known ligands of the arylhydrocarbon receptor. Deletion experiments indicate physiological roles of the arylhydrocarbon receptor during development and for the function of various organs. During early pregnancy, the arylhydrocarbon receptor is specifically expressed in pre-implantation embryos, during blastocyst differentiation and implantation, in the endometrial epithelium and in the decidua cells of the placenta. Coplanar polychlorinated biphenyls were found to be embryotoxic in low doses, i.e. in doses found in tissues of not specifically exposed individuals originating from xenobiotic environmental background contamination. In initial experiments, low-dose exposure of rabbit blastocysts to coplanar polychlorinated biphenyls in vitro did not induce transcriptional changes of the so-called arylhydrocarbon receptor gene battery. The embryological and toxicological implications of the findings are discussed.