Catechol Estrogens Stimulate Synthesis of Prostaglandins in the Preimplantation Rabbit Blastocyst and Endometrium 1

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Abstract
The influence of estradiol-17.beta. (E2) or catechol estradiols [4-hydroxyestradiol-17.beta. (4-OH-E2) on 2-hydroxyestradiol-17.beta. (2-OH-E2)] on prostaglandin (PG) production in the rabbit blastocyst and endometrial cell in vitro on day 6 pregnancy (144 h postcoitum) was studied. Blastocysts (4-6) were incubated in 1 ml of RPMI-1640 medium for a total period of 8 h. Media were changed every 2 h and stored at -80.degree. C. E2, 4-OH-E2 or 2-OH-E2 at various concentrations were added during the 2nd and 4th periods, while the vehicle was added during the 1st and 3rd periods. Single cell suspensions of endometrial tissues in 0.5 ml of RPMI-1640 were incubated for 2 h with and without estrogens. The media and cells were separated and stored at -80.degree. C. PG were determined by radioimmunoassay. The results for blastocyst were expressed as the cumulative release of PG over a period of two 2-h incubations of the same experimental conditions (pg/blastocyst per 4 h). The release of PG from the blastocyst was not influenced by 8.8 .mu.M of 4-OH-E2, whereas 44 .mu.M of this steroid stimulated the release of PGE-A by about 25% and PGF by 59% (P < 0.05) over the vehicle-treated controls. The release of PGE-A and PGF in the presence of 44 .mu.M of 2-OH-E2 was stimulated by .apprx. 60% and 37%. E2 at any concentration, either showed none or inhibitory effects on the release of PG from the blastocyst. The production of PG in the endometrial cells (ng/mg protein per 2 h) was stimulated (P < 0.05) in the presence of both 4-OH-E2 or 2-OH-E2 as compared to vehicle-treated controls. 4-OH-E2 at a concentration of either 17.6 .mu.M, 44 .mu.M or 88 .mu.M increased the production of PGF by about 111%, 183% or 221% and PGE-A by 85%, 144% or 212%, respectively, as compared to vehicle-treated controls (PGF; 18.90 .+-. 0.82 and PGE-A: 2.18 .+-. 0.22 ng). The stimulation of PGF production in the endometrial cells by 2-OH-E2 at 17.6 .mu.M or 44 .mu.M concentration was 67% or 100%, while the production of PGE-A was 126% or 179% more over the controls. E2 at various concentrations either showed none or inhibitory effects on the production of PG in the endometrial cells. Catechol estradiols, but not E2, at the dose levels used, stimulate PG production n vitro both in the preimplantation rabbit blastocyst and endometrial cell.