Previous studies have shown that 17α,20β-dihydroxy-4-pregnen-3-one (17α,20β-P) can induce both germinal vesicle breakdown and ovulationin vitro of yellow perch (Perca flavescens) oocytes. The stimulation of ovulation can be blocked by indomethacin and restored by the subsequent addition of several primary prostaglandins (Goetz and Theofan 1979).In the present investigation, medium levels of prostaglandin F (PGF) and E (PGE) were measured by radioimmunoassay duringin vitro 17α,20β-P-induced ovulation of perch oocytes. PGF levels increased significantly (compared to controls) from 30 to 36h of incubation. Hourly samples taken through the time of ovulation revealed that the increase in PGF was very closely correlated to the time of ovulation though it did not preceed it. Cortisol, testosterone, estradiol-17β, 17α,20α-dihydroxy-4-pregnen-3-one and 17α-hydorxyprogesterone did not increase PGF levels by 48h of incubation, however, several other progestational steroids including 20β-dihydroprogesterone (20β-P) and progesterone did. 17α,20β-P, 20β-P and progesterone also stimulated an increase in PGF in spontaneously ovulating oocytes (in which all oocytes ovulated including controls), indicating that the increase in PGF was not merely a result of the physical process of ovulation but was related to the presence of the steroid.
The synthesis of prostaglandins (PGs) by several tissue components of brook trout (Salvelinus fontinalis) ovaries was investigated using radiolabeled precursor incorporation and radioimmunoassays for PGE and PGF. PGE2 and PGF2α were synthesized from 14C arachidonic acid (AA) by the follicle walls of mature oocytes. Synthesis was significantly greater in follicles taken postovulation as compared to those sampled prior to germinal vesicle breakdown. However, the most extensive synthesis of PGs occurred with tissue outside of the mature follicles (i.e., extrafollicular[EF]). When incubated with AA, the predominant primary PG produced by this tissue was PGE2. EF tissue could be separated microscopically into two major fractions—immature follicles and stromal tissue. When these tissue fractions were incubated separately with AA the stromal fraction retained the ability to produce PGE2, while the immature follicles increased synthesis of PGF2α. 14C‐Eicosatrienoic acid was converted to PGE1 and PGF1α by EF tissue but in significantly reduced quantities relative to AA. Fatty acid analysis indicated that there were significant quantities of arachidonic, eicosapentaenoic, and docosahexaenoic acids in both follicles and EF tissue, but there was not a significant difference between the two tissues in the absolute amount of arachidonate/mg tissue.
In experiments using radioimmunoassays (RIAs), the highest quantities of PGE were measured in incubates containing EF tissue. This supported the results obtained through arachidonic acid incorporation and suggested that this tissue is the primary source of PGE in the brook trout ovary. In contrast, the mature follicules that were undergoing ovulation in vitro produced significant quantities of PGF, whereas the EF tissue production of PGF, measured by RIA, was very low.
The results clearly indicate that there are several potential sites for PG synthesis within the trout ovary that differ in their capacity to produce E and F prostaglandins.
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