Action of a cyclopropenoid fatty acid on the corpus luteum of pregnant and nonpregnant ewes

The effects of a cyclopropenoid fatty acid on luteal cell function were studied. In experiment 1, pregnant ewes were laparotomized on Day 18 of gestation and ewes with CL in both ovaries were unilaterally ovariectomized. Either 1.09 mg of an extract of Sterculia foetida seeds, containing 750 μg sterculic acid methyl ester (SA, n = 6), or 1.09 mg oleic acid methyl ester (OA, n = 6) was injected into the artery supplying the ovary bearing CL. Jugular blood was collected on Day 18 before surgery and daily thereafter until Day 30 of gestation or until detection of estrus, whichever occurred first. Serum was assayed for progesterone (P₄) by RIA. In experiment 2, CL were removed from ewes on Day 10 of the estrous cycle and slices of luteal tissue were incubated in medium containing 145 ng/ml of S. foetida extract (100 ng/ml SA) or 145 ng/ml OA (control) for 90 min. Then tissue was washed and reincubated in medium containing 25 μg 22(R)-hydroxycholesterol/ml or 25 μg pregnenolone/ml for 120 min. Tissue plus medium was analyzed for P₄. Injection of SA or OA on Day 18 of gestation reduced (p < 0.01) serum levels of P₄ within 24 h; concentrations of P₄ then remained low, and relatively constant, in six OA control ewes that were pregnant until Day 30 of gestation and in three SA-treated ewes that had nonviable fetuses on Day 30. Serum concentrations of P₄ in SA-treated ewes were lower than those of control ewes (p = 0.009). The remaining three ewes injected with SA exhibited estrus within 3 to 5 days after treatment. Luteal tissue subjected to SA or OA in vitro did not differ in ability to synthesize P₄ during subsequent incubation in the absence of added precursor substrate (incubated controls). P₄ synthesis by tissue previously exposed to SA or OA, compared with that in the corresponding incubated controls, was not altered by incubation with 22(R)-hydroxycholesterol. Pregnenolone significantly increased P₁ synthesis by luteal tissue incubated with SA or OA compared with that of controls. However, response of SA-treated tissue to pregnenolone was less than that of tissue exposed to OA (p < 0.01). The results of this study suggest that SA can suppress luteal P₄ production or cause luteolysis of CL in ewes during early gestation. The in vivo suppressive effect of SA on the CL may involve its ability to interfere with the conversion of pregnenolone to P₄.