Abstract
Absorption of estrogen by an antiserum against estradiol (ASE) and replacement with diethylstilbestrol (DES) were used to study the role of the early preovulatory rise of estrogen during delayed ovulation on the subsequent increase in abnormal morphological development of the embryos. The study contained 4 treatment groups: control, pentobarbital sodium (Nembutal)-induced delay of ovulation for 48 h; delay of ovulation plus ASE treatment on the first 2 days of the estrous cycle; and DES treatment during the first 2 days of the cycle in addition to treatment with ASE and delay of ovulation. The ASE used did not bind DES. Following mating, rats were killed at day 4 (blastocyst stage) or day 11 (midgestation) to assess embryo development. A 48 h delay of ovulation, as reported previously, produced abnormal development and retarded growth of the embryos at both stages of development (P < 0.05). Implantation rate was decreased, while embryonic death was increased (P < 0.05). All of these detrimental effects were reversed by ASE, while DES reinitiated these events in ASE treated rats. The early rise or prolonged elevation of preovulatory levels of estrogen in relation to the time of ovulation may be responsible for alterations in the oocyte and intrauterine environment which result in subsequent abnormal development and embryonic death following delayed ovulation.