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V. Rider and R. B. Heap

Summary. Early embryo development and implantation were arrested in ferrets passively immunized with a mouse monoclonal anti-progesterone antibody injected intraperitoneally at 72 and 96 h post coitum (p.c.) or at 72 h p.c. only. In control ferrets injected with mouse serum or 0·9% NaCl, implantation sites were found in all mated females; autopsies were carried out at Day 14 p.c. A total of 34 unimplanted embryos were recovered from the reproductive tract of antibody-treated ferrets and none of these had progressed to the blastocyst stage.

When ferrets were treated with antibody at 72 h p.c. and autopsies were carried out at Day 6p.c., only 1 of 29 embryos recovered had progressed beyond the 4-cell stage in 4 females. In 4 control animals most embryos recovered at Day 6 were at the morula (32%) or blastocyst (28%) stage. Embryos from ferrets treated with antibody were therefore developmentally arrested when recovered 72 h after antibody administration.

Plasma progesterone concentrations were ∼ 6-fold higher in antibody-treated ferrets with unimplanted embryos (711 ± 132 nmol/l; 223 ng/ml) compared with control pregnant females (102 ± 4 nmol/l; 32 ng/ml) at Day 14 p.c. The results are consistent with the hypothesis that the normal course of pregnancy is arrested as a result of antibody binding of progesterone in the circulation, presumably causing a decrease in the amount of progesterone available to target cell receptors, and that heterologous anti-progesterone antibody blocks normal cleavage and embryonic development at an early stage before cavitation.

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V. Rider, R. B. Heap, M.-Y. Wang, and A. Feinstein

Summary. Pregnancy was blocked by anti-progesterone monoclonal antibody in two inbred (BALB/cJ, CBA/Ca) but to a lesser degree in an F1 hybrid (CBA/Ca ♂ × BALB/cJ ♀) or an outbred (Tuck's no. 1) stock of mice when antibody was injected intraperitoneally (i.p.) at 32 h post coitum (p.c.) using a dosage of 9·5–10·9 nmol. This different antifertility effect could not be explained solely by altered tubal transport in inbred mice since the rate of transport was slightly accelerated in one stock (BALB/c) but not in another (CBA). In crossbred mice tubal transport was not significantly altered by antibody treatment.

At Day 3 (54–58 h p.c.), the majority of embryos in control mice were at the 4-cell and 8-cell to morula stages in inbred and crossbred stock, respectively, but after antibody treatment they were mainly at the 4-cell stage in all 4 stocks. At Day 4 (78–82 h p.c.) the majority of embryos in control females had reached the blastocyst stage in all stocks, whereas after antibody treatment they had reached this stage in crossbred stock and relatively few had progressed so far in inbred stock.

The results indicate that there are two events in early gestation which are susceptible to passive immunization with anti-progesterone monoclonal antibody. The first of these occurs during cleavage shortly after the 4-cell stage when embryo development was arrested in two inbred stocks of mice. Antibody effects on cleavage were not direct since embryos cultured in the presence of high concentrations of antibody, or antibody saturated with progesterone, continued to develop in the normal way and formed blastocysts. The second event is the onset of implantation, an effect also influenced by genotype. The decidual cell reaction induced by intraluminal oil injection was blocked by antibody injected at 8 or 32 h p.c. in BALB/c females, but only when injected at 8 h, and not at 32 h p.c., in F1 hybrid females. The results show that there is a greater resistance in two crossbred stocks compared with two inbred stocks to the effects of passive immunization against progesterone in early pregnancy.