Granulosa, theca and corpus luteum cells of the goat ovary were isolated and incubated separately for 6 hours, with or without various modulators. Arachidonic acid (AA, 10 ng to 100 μg/ml), the precursor for prostaglandin synthesis, produced a dose-dependent increase in progesterone (P4) and estradiol-17β (E2) productin by all the cell types. Prostaglandin synthetase inhibitors, aspirin (10-6-10-3M) and indomethacin (100 ng-1 mg/ml), produced a dose-dependent decrease in arachidonic acid-stimulated (100 μ/ml) steroid production. Prostacyclin synthetase stimulators, trapidil (1.6 μg- 1 mg/ml) and dipyridamole (10-6-10-3M), when added alone or along with AA, did not effect steroid production. Up to 100 μg/ml of U-51605 (9,11-azoprosta-5, 13-dienoic acid), a prostacyclin synthetase inhibitor, did not inhibit basal or AA-stimulated steroid production. Prostacyclin (PGl2) and its stable analog 6βPGl1(0.01-10μg/ml) produced a dose-dependent increase in P4 and E2 production in all three cell types. Increase at 1 and 10μg/ml was significant in all cases. 6-keto-PGE1 (an active metabolite of PGl2 in certain systems) produced an increase in steroid production which was significant in theca at ≥ 1μg/ml concentrations but had no significant effect on granulosa and corpus luteum cells at any dose level. 6-keto-PGf1 alpha (stable metabolite of PGl2) was without effect inthe present system. The lack of effect of PGl2 at lower concentrations was not altered by either differentiation of the cells with FSH and testosterone or addition of steroid precursors, testosterone and pregnenolene. The present results indicate that AA- stimualted steroid production in the goat ovarian cell type is mediated by prostaglandins other than PGl2 though PGl2 itself can positively modulate the steroid production.
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