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Estrogenic steroids regulate cellular function in a wide variety of tissues [ 1 ] . During human pregnancy, the production of 17-beta-estradiol (E2) rises eighty fold, from 0.75 nM preovulatory peak to 60 nM at term [ 2 3 4 5 ] , and estrogens influence various aspects of placental function and fetal development in humans and primates [ 6 7 8 9 10 11 12 ] . Several previous studies have shown that human placenta binds estradiol [ 13 14 15 ] . However, more recent immunohistochemical studies on paraffin-embedded or snap frozen sections as well as other techniques (RT-PCR for ER-alpha mRNA) failed to demonstrate estrogen receptor alpha (ERα) in human placentae during pregnancy or in cultures of dispersed placental cells [ 16 17 ] . However, it has been indicated that the failure to detect the ERα does not entirely preclude the presence of this receptor in human trophoblast cells, but might be attributed to a relatively low number and density of ERα molecules on these cells [ 17 ] . On the other hand, Billiar et al.