[The metabolism and conjugation of estrogens in the human fetus].

Although several studies have been reported on the synthesis of steroids in the fetus, the metabolism and conjugation of estrogens in the fetus is not completely known. In this study serum levels of estetrol (E4), estetrol glucosiduronate (E4-G), estriol (E3) and estriol-16-glucosiduronate (E3-16-G) were measured by R.I.A. in maternal peripheral vein blood (MPV), umbilical artery blood (UA) and umbilical vein blood (UV) at delivery. The same steroids were also measured in various fetal organs (liver, kidney, intestine, adrenal, lung and placenta) in the second-trimester. After 4-14C-E2, 4-14C-E3 and 6, 9 (n)-3H-E4 were incubated with homogenates of various human fetal organs, the metabolites were analyzed with an authentic sample. 15, 15-D2-estradiol-17 beta (d2-E2) was incubated with human second-trimester fetal liver and the metabolites were analyzed with GC-MS. It was concluded that: 1) E3-16-G was higher in UA and UV than in MPV, suggesting active glucosiduronation in the fetus. 2) Higher levels of E4 and E4-G in UA and UV than in MPV suggest the production of E3 and E3-16-G in the fetus. 3) Levels of E4 and E4-G were higher than those of E3 and E3-16-G in various fetal organs in the second-trimester. 4) E4 and E4-G were especially high in fetal liver and intestine, and E3 and E3-16-G were high in fetal kidney, liver and intestine. 5) The level of E3-16-G was higher than that of E3 in these organs. 6) The second-trimester fetal liver conjugated E2, E3 and E4 to each glucosiduronate. 7) The second-trimester fetal kidney conjugated E2 and E4 to each sulfate, but E3 to E3-16-G. 8) 15-Hydroxylation of d2-E2 was demonstrated in the incubation with homogenate of second human fetal liver. 9) The active glucosiduronation of E3 in the fetus was thought to inactivate a large amount of E3 transported from the placenta.