Oestradiol-17\g=b\ was produced by cultures of 5-and 6-day rabbit blastocysts containing 0\m=.\5\p=n-\1 \g=m\M-[3H]testosterone. Addition of the aromatase inhibitor 4-hydroxy-4-androstene-3,17-dione at 3\m=.\5\p=n-\7um reduced oestradiol production by 66\p=n-\73% but had no effect on the size of blastocyst. Injection of 6 mg 4-OH-androstenedione or 5\p=n-\10 mg 4-acetoxy-4-androstene-3,17-dione, into the uterine lumen on Day 5 did not interfere with implantation. The functional significance of blastocyst oestrogen in rabbit remains obscure.

When Day 5 rat blastocysts and Day 4 and 5 mouse blastocysts were cultured in 53 microliters of medium containing 1340 or 2680 pg [3H]estradiol (E2), large amounts of [3H]estrone (E1) were detected in the medium at daily intervals for up to 5 days. This indicates the presence of 17 beta-hydroxysteroid dehydrogenase in the embryos. The activity was higher at a higher concentration of E2 and was also higher in mouse than in rat blastocysts. In the mouse, the activity was higher in Day 5 than Day 4 blastocysts during the first day in culture; then it decreased in Day 5 but increased in Day 4 blastocysts. The importance of E2 in embryonic development and implantation as suggested by others may be related to the activity of 17 beta-hydroxysteroid dehydrogenase.

No abstract

Following the finding of 17 beta-hydroxysteroid dehydrogenase activity in mouse blastocysts, the present study examined the relation of estrone (E1) production rate to estradiol-17 beta (E2) concentration in the medium. When Day 5 blastocysts were cultured in 107-6,860 ng E2/ml medium, the amount of E1 formed during the first 5 hours (y) was found to increase linearly with the logarithm of E2 concentration (x), as represented by the equation y = 2,161x - 3,947. However, there was a sharp decline during the next 5 hours of culture except for the 107 ng E2 culture. The E1 production then remained steady for up to 46-58 hours. There was a tendency for further decline during the 46-70-hour period. The results indicate that (1) E2 may be metabolized to E1 and, probably, another unknown steroid; (2) E1 production rate is E2-dose dependent; and (3) the blastocyst possesses the enzymatic capability to change the steroid milieu to suit its own needs and/or to cause local effects in the uterus for its proper implantation.