Dorothy M. Hunt

Effect of prostaglandin F2α on ovulation and fertilization in rabbit

Abstract The effect of prostaglandin F 2α on ovulation and fertilization was studied in rabbits. The number of ovulation was not affected by subcutaneous injection of PGF 2α but the recovery of ova was significantly decreased when PGF 2α was given either at 12 or 16 h after HCG injection and autopsied 24 h latter. The results suggest that exogenous PGF 2α accelerates ovum transport and expels the eggs prematurely from the female tract and does not impair ovulation or the fertilization processes when given to rabbit at 1 mg/kg B.W.

Suppression of Pregnancy in the Rabbit by Subcutaneous Implantation of Silastic Tubes Containing Various Estrogenic Compounds

This study attempts to find out: 1) whether normal fertility can be resumed after the removal of subcutaneous implants containing various estrogenic compounds; 2) whether other compounds with estrogenic activities have such effects; and 3) whether such effect is on the embryo or the female tract. 10-mm long sealed silastic tubes were used to implant .5 or 2 mg of ethinyl estradiol (EE) diethylstilbestrol or quinestrol (ethinyl estradiol 3-cyclopentyl ether) under the skin in the neck region of adult rabbits. Subsequently the rabbits were bred or inseminated. Fertility reverted to normal after removal of .5 or 2 mg of ethinyl estradiol implanted for 42 days. After 10 to 25 days of implantation of .5 mg stilbestrol 17-21% of eggs developed into normal blastocysts and embryos but none developed after implantation of 2 mg of stilbestrol. When animals were inseminated 31 days after stilbestrol implantation no eggs developed into embryos although 14% developed into blastocysts. Insemination 10-25 days after implantation of 2 mg quinestrol resulted in a complete degeneration of eggs but after 33 days 47% of the eggs developed into normal blastocysts and 61% into normal embryos. When early blastocysts recovered from estrogen-treated rabbits were transferred to the uteri of untreated rabbits development of embryos occurred; when transferred from untreated to treated rabbits none developed into embryos. Compounds with estrogenic activity are thought to cause degeneration of eggs by too fast or too slow transport from the tube to the uterus and also to cause a hostility of the uterus to early blastocysts. The effectiveness of estrogens to prevent pregnancy is dependent upon the compound the dosage and the absorption rate of the compound.

Endocrinological and Physiological Features after Steroid Treatment of Male Rats

The effects of medroxyprogesterone acetate (Provera), testosterone propionate (TP), ethinyl estradiol (EE), and ethynodiol diacetate (ED) treatments on sperm population in different segments of the male rat reproductive tract, reproductive organ weights, circulating androgens and fertility were studied. Ten microgram TP given for five days reduced the sperm population and organ weights. A marked reduction in the number of sperm and reproductive organ weights was observed in males orally treated with estrogens. Only long-term (20 days) treatment with Provera (1 mg/day) significantly reduced sperm population and reproductive organ weights. Combination of TP and Provera resulted in a more pronounced reduction in sperm counts and organ weights. Among steroids studied, estrogen was the only compound which suppressed fertility and circulating steroid levels.

Effects of Estradiol-17/β on Reproduction in Adult Male Rats

Estradiol-17 beta (E2-17 beta) treatment induced dose-related reduction of sperm population and eventual azoospermia, atrophy of accessory organs, and suppressed serum LH and testosterone levels. In spite of all these alterations mating behavior was not affected, although the number of implantation sites paralleled the reduction of sperm population, suggesting that the primary detectable response to E2-17 beta treatment is related to the steroidogenic components of the testis and the hypothalamic pituitary axis. The duration of treatment is more critical for the induction of azoospermia in the rat than the total dose of E2-17 beta.