Premature luteal regression induced by equine chorionic gonadotropin and estrogen is suppressed by administration of exogenous interferon in red deer (Cervus elaphus)

Superovulation of red deer hinds with eCG causes premature luteal regression by inducing follicular hypersecretion of estrogen that activates the luteolytic mechanism. Six groups of hinds (n = 8 per group) were treated with progesterone-impregnated intravaginal controlled internal drug-releasing (CIDR) devices for 14 days to synchronize estrus (CIDR device withdrawal = Day 0). Group 1 served as controls; group 2 received an i.m. injection of 1200 IU eCG at -72 h; group 3 received similar eCG treatment as well as i.m. injections of 0.25 mg estradiol benzoate (EDB) at 72, 84, 96, and 108 h; group 4 received twice-daily i.m. injections of 4 mg recombinant bovine interferon-(alpha)(I)1 (IFN) from Days 2 to 7; group 5 received IFN and eCG as above; group 6 received IFN, eCG, and EDB. Ovarian response was determined by laparoscopy on Days 14 and 15. Progesterone profiles were determined from thriceweekly plasma samples from Days -14 to 28. Both the incidence of visible signs of luteal regression and the variation in the time of termination of the luteal phase (plasma progesterone < 1 ng/ml) were greater in eCG+EDB-treated hinds than in control, IFN-, IFN+eCG -, and IFN+eCG+EDB-treated hinds (p < 0.05). The ovulation rate in the eCG+EDB-treated hinds was less than that in the eCG-, IFN+eCG-, and IFN+eCG+EDB-treated hinds (p < 0.05). These results suggest that treatment with interferon, the putative embryonic pregnancy recognition signal, suppresses premature luteal regression induced by hypersecretion of estrogen following treatment with eCG.