Experiments were conducted to examine the effect of a cyclopropenoid fatty acid (CPFA) on progesterone (P4) production by the ovine corpus luteum (CL) during the estrous cycle. Ewes in Exp 1 and 2 were laparotomized on day 2 of the estrous cycle, and animals with CL in both ovaries were subjected to unilateral ovariectomy. Ewes with CL in one ovary only were not ovariectomized. During surgery, ewes were injected with a mixture of fatty acids (sterculic acid, 39%; palmitic, 29%; linoleic, 12%; malvalic acid, 9%; oleic, 8%; stearic, 3%) containing 500 μg sterculic acid (SA; Exp 1), 750 μg SA, or 750 μg oleic acid (Exp 2) via the artery supplying the ovary bearing the CL. Control ewes were similarly injected with vehicle only (0.1-0.2 ml dimethylsulfoxide; Exp 1 and 2, respectively). Sera from blood samples collected at 15-min intervals for 1 h after injection or once daily on alternate days of the cycle after surgery were analyzed for LH and P4, respectively. In Exp 3, slices of CL removed from five ewes on day 10 of the cycle were incubated for 90 min in medium containing 100 ng/ml SA or vehicle (10 μl dimethylsulfoxide). Slices were then reincubated for 90 min in medium containing 10 ng/ml oLH or saline (10 μl). Tissue and medium were analyzed for P4. Injection of 500 μg SA suppressed serum levels of P4(P < 0.01), but did not alter mean cycle length. Injection of 750 μg SA reduced serum concentrations of P4 and shortened estrous cycle duration (P < 0.005). Oleic acid (750 μg) or as much as 1.9 mg of a mixture of fatty acids devoid of CPFA had no effect on cycle length or serum levels of P4, suggesting that altered luteal function was due to the type and not the quantity of fatty acid injected. Treatments had no effect on serum concentrations of LH. Preincubation with SA interfered with the ability of luteal slices to synthesize P4when subsequently incubated alone or with ovine LH (P < 0.01). It is concluded that SA acts on the CL to impair steroidogenesis and ultimately cause luteal regression.
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