ABSTRACT
Experiments were performed to determine the mechanism by which recombinant bovine interferon-αI1 (rbIFN-α) causes an acute reduction in plasma concentrations of progesterone. In experiment 1, administration of a prostaglandin synthesis inhibitor blocked rbIFN-α-induced hyperthermia but did not prevent the decline in plasma concentrations of progesterone. The decline in progesterone concentrations caused by rbIFN-α was, therefore, not a direct consequence of the associated hyperthermia or of pathways mediated through prostaglandin synthesis. It is also unlikely that rbIFN-α acts to increase the clearance of progesterone since injection of rbIFN-α did not decrease plasma concentrations of progesterone in ovariectomized cows given an intravaginal implant of progesterone (experiment 2). In experiment 3, rbIFN-α did not affect basal and LH-induced release of progesterone from cultured luteal slices, indicating that rbIFN-α is unlikely to affect luteal function directly. Injection of rbIFN-α did, however, cause a decrease in plasma concentrations of LH in ovariectomized cows (experiment 4) that coincided temporally with the decrease in progesterone concentrations seen in cows having a functional corpus luteum. The present results strongly suggest that rbIFN-α acts to reduce secretion of progesterone by interfering with pituitary support for luteal synthesis of progesterone. The finding that rbIFN-α can inhibit LH secretion implies that interferon-α molecules should be considered among the cytokines that can regulate hypothalamic or pituitary function.
Journal of Endocrinology (1992) 133, 175–182
A nonhormonal model for emergency contraception: prostaglandin synthesis inhibitor effects on luteal function and lifespan, a pilot study
