| Summary: | Two experiments were conducted to examine the effect of
a cyclopropenoid fatty acid on luteal cell function. In Exp.
1, 12 mature ewes were mated to a fertile ram, assigned to two
groups (n = 6/group) and laparotomized on day 18 of gestation.
Ewes with corpora lutea (CL) in both ovaries were unilaterally
ovariectomized while ewes with a CL in one ovary only were
allowed to remain intact. An extract of Sterculia foetida
seeds (1.09 mg), consisting of a mixture of fatty acid methyl
esters including 750 ug of sterculic acid (SA), or 1.09 mg
oleic acid methyl ester (OA) 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 detected estrus, whichever occurred first.
Sera were assayed for progesterone (P₄) by radioimmunoassay.
In Exp. 2, 12 mature ewes were laparotomized on day 10 of the
estrous cycle and CL were removed, weighed and sliced for
incubation. Corpora lutea from two ewes were pooled for each
incubation. Slices of CL were preincubated in medium
containing 145 ng/ml of S. foetida extract (100 ng/ml
sterculic acid methyl ester) or 145 ng/ml oleic acid methyl
ester (control) for 90 min. Then, slices of tissue were
washed and reincubated in fresh medium containing 25 ug 22(R)-
hydroxycholesterol/ml (0.079 nM final concentration) or 25 ug
5-pregnen-3βol-20-one/m1 (0.084 nM final concentration) for
120 min. Tissue plus medium were analyzed for P₄. Injection
of SA or OA on day 18 of gestation caused a reduction in serum
concentrations of P4 within 24 h, after which concentrations
of steroid remained low and relatively constant in control and
those SA-treated ewes that remained pregnant until day 30 of
gestation. Three of six ewes that were injected with SA
exhibited estrus within 3 to 5 days after treatment. Serum
concentrations of P₄ of SA-treated ewes differed from those of
OA-injected control ewes (P<0.01). Luteal tissue subjected
to SA or OA in vitro did not differ in ability to synthesize
P₄ during subsequent incubation in the absence of precursor
substrate (incubated controls). Relative to respective
incubated controls, P₄ synthesis by tissue previously exposed
to SA or OA was not altered by incubation in the presence of
22(R)-hydroxycholesterol. Presence of 5-pregnen-3βol-20-one
(pregnenolone) in the medium significantly increased P₄
synthesis by luteal tissue preincubated with SA or OA compared
with that of controls. However, response of SA-treated tissue
was markedly less than that of tissue exposed to OA (P<0.05).
Results of this study suggest that $A can cause
regression of CL in 50% of pregnant ewes. Apparently, the
luteolytic effect of SA may be caused by its ability to
interfere in the conversion of pregnenolone to P₄ by 3β-
hydroxysteroid dehydrogenase. === Graduation date: 1991
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