Effects of Ethinyl Estradiol on Egg Transport and Development in the Rabbit

Publisher Website
Google Scholar
Abstract
A total of 251 mature female rabbits was used in this study. One hundred eight of these were divided into groups of 6 and orally dosed at 24, 48 and 72 hr. after insemination and injection of human chorionic gonadotrophin (HCG), with graded doses of various estrogens [stilbestrol, estradiol cyclopentylpropionate (ECP), estrone, estradiol and ethinyl estradiol (EE)], dissolved in 1 ml cottonseed oil. The eggs were recovered on day 6, and classified according to their development. EE was found to be the most effective estrogen in preventing normal blastocyst development. The ED50 (and its 95% probability limits) was 0.012 (0.010-0.014) mg/rabbit/day. EE was therefore used in the remainder of the study. Eighteen rabbits were given a single dose of 0.05 mg EE at 24, 48 or 72 hr. after insemination and injection of HCG and no significant differences in the percentage of blastocyst development was found. This dose given at 24 hr. was found to be as effective as a total dose of 0.048 mg EE given over 3 days in reducing blastocyst development by 64%. Ninety-nine rabbits were given graded doseses of EE orally at 24 hr. after insemination and injection of HCG. They were killed at 48 or 72 hr. The eggs were recovered from the different sections of the oviducts, uteri and vaginae. It was found that as the dose of EE increased the percentage of eggs remaining in the oviduct at 48 hr. decreased significantly. No such decrease was observed at 72 hr., since only 29% of eggs remained in the oviducts of control animals at this time. In both 48- and 72-hr. groups the position of those eggs remaining in the oviducts was altered. The percentage of eggs found in the ampulla or at the junction of the ampulla and isthmus increased as the dose of EE increased to 0.5 mg, probably due to the occlusive effect of estrogen on the isthmic musculature. Eggs examined at 48 or 72 hr. after insemination were not delayed in development compared to eggs from control animals, irrespective of the dose of estrogen administered or the site of recovery from the genital tract. However, a single dose of 0.05 mg EE at 24 hr. has been shown to reduce blastocyst development on day 6 to 36% of normal. A further experiment involving transfer of eggs from 10 estrogen-treated donors to 4 untreated recipients, and from 6 untreated donors to 6 recipients which had received the same dose of EE, was performed. No differences in development were observed irrespective of whether the egg or the endometrium has been treated with estrogen. It was therefore concluded that estrogen interferes with egg development by disturbing egg transport. Thus, the eggs enter the uterus too soon or are left in the oviduct too long.

This publication has 1 reference indexed in Scilit: