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Antenatal glucocorticoid administration is used in cases of fetuses at risk to be born prematurely to enhancefetal pulmonary surfactant production and prevent infant respiratory distress syndrome. The CYP1A1 isthe most important xenobiotic-metabolizing cytochrome P450 enzyme in the human placenta. Importantly,CYP1A1 generates reactive species and its placental activity is elevated in smoking women. CYP1A1expression is mainly controlled by aryl hydrocarbon receptor (AHR) ligands. Glucocorticoid co-regulationof CYP1A1 has been described in various cell types but has not been systematically examined in the humanplacental trophoblast.We studied the effects of the glucocorticoids dexamethasone and betamethasone on inducibility ofCYP1A1 and other AHR target genes CYP1A2, CYP1B1, UGT1A1 (UDP-glucuronosyltransferase 1A1) andBCRP (Breast cancer resistance protein) by prototype AHR ligand 3-methylcholanthrene (3MC) in isolatedhuman placental trophoblast culture.We show that glucocorticoids alone had no effect on activity and protein/mRNA expression of CYP1A1and little effect on mRNA expression of other AHR target genes. However, glucocorticoids significantlystimulated CYP1A1 mRNA, but not CYP1A2, CYP1B1, UGT1A1 and BCRP mRNAs, induction mediatedby the AHR ligand. Consistently, glucocorticoids significantly augmented 7-ethoxyresorufin-O-deethylation(EROD) enzymatic activity in primary human placental trophoblast. Dexamethasone did not influence AHRand ARNT (Aryl hydrocarbon receptor nuclear translocator) mRNAs, suggesting that this phenomenon isnot due to AHR or ARNT up-regulation by glucocorticoids in human trophoblast.In conclusion, our data suggest that glucocorticoids have no effect on AHR target genes expression perse, but they may potentiate CYP1A1 induction in human term placental trophoblast

Effects of glucocorticoids on cytochrome P450 1A1 (CYP1A1) expression in isolated human placental trophoblast