PGF Levels Research Articles

The effect of dietary lipid on polyunsaturated fatty acid metabolism in Atlantic salmon (Salmo salar) undergoing parr-smolt transformation.

The aim of this study was to measure the changes in lipid metabolism which occur during smoltification and seawater transfer in Atlantic salmon (Salmo salar). Duplicate groups of Atlantic salmon parr were fed diets containing either fish oil (FO) or a blend of linseed and rapeseed oils, vegetable oil (VO), from October (week 0) to seawater transfer in May (week 26). From May to August (weeks 26-43), all fish were fed a fish oil-containing diet. Fatty acyl desaturation and elongation activity were followed in isolated hepatocytes incubated with radioactive 18:3n-3 and 18:2n-6. Metabolism of 18:3n-3 was consistently around 5-fold greater than metabolism of 18:2n-6, and total metabolism of both substrate polyunsaturated fatty acids (PUFA) was increased in fish fed both VO and FO up to seawater transfer after which desaturation activities were reduced. Desaturation activities with both 18:3n-3 and 18:2n-6 were significantly greater in fish fed VO, compared to fish fed FO, at 22 and 26 wk. Arachidonic acid (20:4n-6; AA) in liver polar lipids (PL) of fish fed VO increased consistently from weeks 0-22 but varied after seawater transfer. In fish fed FO, AA in liver PL remained constant up to week 17 before increasing at seawater transfer and leveling off thereafter. Eicosapentaenoic acid (20:5n-3; EPA) in liver PL of fish fed VO decreased significantly from week 0-22 before rising at seawater transfer and increasing rapidly posttransfer. EPA in liver PL of fish fed FO showed a similar trend except EPA was always greater in the freshwater phase compared to fish fed VO. Docosahexaenoic acid (DHA) levels in liver PL of fish fed VO remained constant in the seawater phase before increasing following seawater transfer. In fish fed FO, DHA in liver PL increased from weeks 0-17 reducing and leveling off postseawater transfer. The levels of PGF(2 alpha) and PGF(3 alpha) were measured in isolated gill cells stimulated with calcium ionophore A23187. PGF(2 alpha) production in fish fed VO increased significantly between 0-7 wk before decreasing toward seawater transfer. After transfer, PGF(2 alpha), production increased to a peak at 35 wk. PGF(2 alpha) production in fish fed FO was not significantly altered during the trial period. The changes in PGF(3 alpha) production were broadly similar to those occurring with PGF(2 alpha), but the latter was always in excess of the former (2- to 4-fold). Plasma chloride concentrations in fish subjected to seawater challenge at 20 wk were significantly lower in fish fed VO compared to those fed FO. This study has provided new information on the changes in lipid metabolism which accompany parr-smolt transformation and suggests that diets which have a fatty acid composition more similar to that in aquatic invertebrates may be beneficial in effecting successful seawater adaptation.

Prostaglandins and ovum implantation in mice

The possible involvement of prostaglandins (PGs) in events of ovum implantation is investigated. The levels of PGF and PGE-A were measured by radioimmunoassay in the implantation and interimplantation sites on days 4, 5, 6, and 7 of pregnancy. The concentration of prostaglandins was determined in morulae and blastocysts also. The levels of PGE-A were higher in implantation sites in comparison to PGF. PGE-A level showed a peak on d5 and remained significantly higher on d6 and d7, in comparison to d4. The concentration of PGF was found to be very low in both interimplantation sites and implantation sites before implantation. The concentration of PGF showed a significant increase on d6 in the interimplantation sites which peaked up to 32.61 +/- 2.01 ng on d7. The embryos showed an increase in PGE-A concentration along with development. However, PGF could not be found in the embryos. The present result shows that in mice PGE is the main prostaglandin involved in ovum implantation and PGF is associated with maintaining the embryos in the uterus. It is also predicted that in mice, blastocysts differentially stimulate PG synthesis in the uterus between implantation sites and interimplantation sites.

The ovarian regulation of ovulation in teleost fish

Ovulation is the release of a mature oocyte from its follicle wall enclosure in the ovary. This process requires the separation of the oocyte from the granulosa layer, the rupture of the follicle wall and the active expulsion of the oocyte through the rupture site. Results of experiments on various vertebrates, including fish, have shown that the control of these processes may involve the cooperative action of a number of ovarian regulators including proteases, protease inhibitors, progestational steroids, eicosanoids, catecholamines and vasoactive peptides. We have used two teleost models, the brook trout (Salvelinus fontinalis) and the yellow perch (Perca flavescens) to study the mechanism and control of ovulation in fish. Using subtractive cDNA cloning, a family of ovarian and ovulation specific mRNAs (“TOPs” = trout ovulatory proteins) was isolated from the brook trout ovary. These mRNAs have not previously been observed in the ovary of any vertebrate species; however, the proteins they code for have significant sequence homology to a group of mammalian protease inhibitors called antileukoproteinases. These inhibitors have been isolated from several mammalian mucosal tissues and their function may be to protect the mucosal lining from nonspecific degradation by proteases released from infiltrating leukocytes. The ovarian proteins encoded by the TOP mRNAs have now been characterized by Western blotting using antibodies derived against recombinant TOPs. Given the similarity of TOPs to antileukoproteinases, one function of TOPs may be to regulate proteolysis at the time of ovulation. In yellow perch, the maturational steroid, 17α,20β-dihydroxy-4-pregnen-3-one (17,20-PG), stimulates both germinal vesicle breakdown and ovulation in vitro. The stimulation of ovulation can be blocked by indomethacin, a prostaglandin endoperoxide synthase inhibitor. Thus, it appears that 17,20-PG acts through the production of an eicosanoid that is most likely a primary prostaglandin. This hypothesis is further supported by the observations that (1) a direct correlation exists between indomethacin levels that block ovulation and those that block primary prostaglandin synthesis in the ovary; (2) ovulation can be restored in indomethacin-blocked incubates with primary prostaglandins; (3) PGF levels increase at the time of ovulation in incubations of yellow perch follicles stimulated with 17,20-PG; and (4) the stimulation of PGF by steroids in the ovary is specific for 17,20-PG. Finally, 17,20-PG-stimulated ovulation and follicular prostaglandin synthesis requires the close interaction of extrafollicular tissue and other follicle wall layers.

Identification of functional high and low affinity states of the prostaglandin F2 alpha receptor in the ovine corpus luteumin vivo and their role in hormone pulsatility

Equivocal evidence has accumulated for the presence of high and low affinity receptors for PGF(2α) in the corpus luteum based on binding affinities of(3)H-PGF(2α) to cell membranes or separated whole cells. Some studies report only high affinity sites, while others report the occurrence of both high and low affinity sites. We have previously demonstrated, using subluteolytic levels of PGF(2α), the existence of functional high affinity luteal PGF(2α) receptors which show desensitization and recovery after 6 to 9 h. The present study, using direct intra-arterial infusions of PGF(2α) into the autotransplanted ovary in conscious sheep, was designed to probe for the existence of functional high and low affinity states of the PGF(2α) receptor in the corpus luteumin vivo. Subluteolytic and luteolytic concentrations of PGF(2α) (100 pg/min and 2500 pg/min, respectively) were infused sequentially, each for 2 h, into the ovary during the luteal phase (n=7 sheep). The same low and high concentrations of the inactive metabolite of PGF(2α) (PGFM) were given over the same time periods as negative controls (n=4 sheep). During the 2 h intra-arterial infusion of 100 pg/min of PGF(2α) the secretion rate of oxytocin increased (P<0.01) while the secretion rate of progesterone was unaffected. In contrast, during the 2 h intra-arterial infusion of 2500 pg/min of PGF(2α), secretion rate of oxytocin increased (P<0.01) and secretion rate of progesterone now began to decline (P<0.05). During the 2 h infusions of identical concent-rations of PGFM, the secretion rate of oxytocin and progesterone remained unchanged. These results indicate the existence of functional high and low affinity states of the PGF(2α) receptor within the ovine corpus luteumin vivo.

Effects of nonsteroidal antiinflammatory drugs on oxidative pathways in A/J mice

The tobacco-specific N-nitrosamine, NNK, is a potent carcinogen in laboratory animals. The authors have shown previously that NNK-induced lung tumorigenesis in A/J mice can be reduced significantly by certain nonsteroidal antiinflammatory drugs (NSAIDs), such as sulindac, ibuprofen, or piroxicam treatments. In this study, the authors investigated whether NSAIDs could reduce NNK-induced oxidative DNA damage and/or inhibit endogenous lipid peroxidation, or prostaglandin E 2 (PGE 2) synthesis in A/J mice. In the first experiment, A/J mice were gavaged with NNK (112 μmol/kg b. w.) three times a week while being maintained on a diet to which either ibuprofen (263 mg/kg diet), naproxen (230 mg/kg), sulindac (123 mg/kg), piroxicam (25 mg/kg), indomethacin (5 mg/kg), or no NSAIDs had been added. Levels of 8-OH-dG in the DNA of lung and liver were measured by high-performance liquid chromatography with electron capture detector. Treatment with NSAIDs had no significant effects on the endogenous or NNK-induced formation of 8-OH-dG in the lung of the mice. In a second experiment, after treatment of A/J mice with NSAIDs for 2 weeks, lipid peroxidation was assayed by determining thiobarbituric acid-reactive substances (TBA-RS) in lung tissues, and prostaglandin E 2 levels were measured in plasma by an enzyme immunoassay. Treatments with some NSAIDs lowered the levels of lipid peroxidation and plasma levels of PGF 2 below basal levels. Taken together, these results suggest that the inhibition of NNK-induced lung tumorigenesis by NSAIDs is more likely related to an inhibition of prostaglandin synthesis than to a direct inhibition of lipid peroxidation or oxidative DNA damage induced by NNK.

A mid-luteal phase comparison of V76 peritoneal fluid volume and its content of PGF 2α and PGE 2 in women with minimal stage endometriosis and a normal pelvis

The study was carried out following the approval of our Hospital Ethics Committee and an informed patient consent. Samples of peritoneal fluid were collected from the Pouch of Douglas at laparoscopy from 32 subjects with minimal stage endometriosis (MSE) and 16 without any visible signs of endometriosis (normal group). All the subjects were in 20 to 23 day period of their menstrual cycle which was histologically confirmed. The endometriosis score was estimated according to the American Fertility Score, 1985 and the fluid samples were collected in tubes containing heparin/indomethacin and standing in ice. The samples were estimated for volume, erythrocyte count, prostaglandin(PG) F 2 α , and PGE 2. Radioimmunoassay techniques were used for the estimation of PGs. Prostaglandin F 2 α , was measured in its parent form while PGE 2 was converted into bicyclic-PGE 2 before estimation. The results indicate that the peritoneal fluid in women with MSE has higher than normal levels of PGF 2 α and lower than normal levels of PGE 2 and its PGE 2 : PGF 2 α ratio is also below normal. There is no difference in the volume of peritoneal fluid in the two groups. Provided the fluid sample is not contaminated with abdominal blood its erythrocyte count is not related to its prostaglandin content.

Regulation of prostaglandin E and F production in the goldfish testis

AbstractThe present studies have investigated the putative role of activators of different signal transduction pathways in the regulation of prostaglandin (PG) production by goldfish testis pieces in vitro. The protein kinase C activator (PKC) phorbol 12‐myristate 13‐acetate (PMA: 1.56‐400 nM) and calcium ionophore A23187 (62.5‐4000 nM) stimulated PGE and F production in a dose and time‐dependent fashion. There was no synergism between A23187 and PMA in stimulating PG production. PGE levels were at least 4.5 times higher than PGF levels. The phorbol ester 4α phorbol didecanoate (400 nM), which does not activate PKC, had no effect on PGE production. The synthetic diacylglycerol 1‐oleoyl‐2‐acetyl‐sn‐glycerol (100 μM), but not 1,2‐dioctanoyl‐sn‐glycerol (100 μ), stimulated PGE production. Although the gonadotropin analog human chorionic gonadotropin (1 IU/ml), adenylate cyclase activator forskolin (2 μM) and testosterone (5 ng/ml) had no effect, the cyclic nucleotide phosphodiesterase inhibitor 3‐isobutyl‐1‐methylxanthine (1 mM) and cyclic adenosine‐3′,5′‐monophosphate analog dibutyryladenosine‐3′,5′‐monophosphate (2 mM) inhibited PMA (400 nM) and A23187 (1 μM)‐stimulated PGE production. PMA and A23187 (400 nM and 1 μM, respectively)‐stimulated PGE production was inhibited by phospholipase A2 inhibitors 4‐bromophenacyl bromide, quinacrine and chloroquine (all 6.25‐400 μM) and by diacylglycerol lipase inhibitor RHC 80267 (10–100 μM), suggesting that both lipases are involved in the release of precursor fatty acids for PG synthesis by goldfish testis tissue. These data, in conjunction with earlier studies showing that PGE stimulates testosterone production by goldfish testis pieces, lend support to the contention that locally produced PGs of the E series modulate testicular steroidogenesis in teleosts. © 1993 Wiley‐Liss, Inc.

Effects of neurohypophyseal and adenohypophyseal hormones, steroids, eicosanoids, and extrafollicular tissue on ovulation in vitro of guppy ( Poecilia reticulata) embryos

In the viviparous guppy, oocyte maturation is followed by intrafollicular fertilization and gestation. The fully developed embryos are ovulated at term just prior to parturition. Various agents were tested in vitro for their effects on ovulation of embryos in isolated follicles of the guppy. Arachidonic acid (10 and 100 μ M), PGE 2, PGF 2α, and 6-keto-PGF 1α (0.1 μg/ml) induced ovulation, while PGE 1, 15-keto-PGF 2α, leukotriene B 4, 5-, 12-, and 15-HETEs (0.01 to 0.1 μg/ml), cortisol, 11-deoxycortisol (25 and 250 ng/ml), estradiol-17β, testosterone, 17α,20β-P, progesterone (5 and 50 ng/ml), isotocin, vasotocin (0.02 to 2 μg/ml), and guppy pituitary extract (one and two glands per fish) did not. Extrafollicular (EF) ovarian tissue cocultured with isolated follicles induced ovulation, and the medium levels of PGE and PGF in such incubations were higher than those in the control. Indomethacin, the cyclooxygenase inhibitor, did not inhibit ovulation induced by arachidonic acid and EF tissue, although it inhibited PGE and PGF production. NDGA, the lipoxygenase inhibitor, did not inhibit ovulation induced by arachidonic acid or EF tissue. A combination of eicosanoids synthesized by follicles and EF tissue may be involved in the induction of ovulation. Dibutyryl cAMP inhibited ovulation induced by PGE 2, PGF 2α, 6-keto-PGF 1α, and EF tissue suggesting that a low level of cAMP may be associated with ovulation in the guppy.

Sodium orthovanadate induces in vitro ovulation and ovarian prostaglandin synthesis in brook trout (Salvelinus fontinalis)

The in vitro effects of sodium orthovanadate (Na3VO4), a G-protein activator, on ovulation and prostaglandin (PG) synthesis were investigated in the brook trout (Salvelinus fontinalis) ovary. PGE and PGF levels in incubation medium of either extrafollicular (EF) tissue or follicles were measured by specific radioimmunoassays (RIA). PGE levels in follicle incubates were increased by Na3VO4 at both pre-germinal vesicle breakdown (preGVBD) and preovulatory (preOV) stages. However, an increase of PGF levels in follicle incubates was observed only in preGVBD follicles in the presence of Na3VO4. The preOV follicles spontaneously released more PGF than preGVBD follicles and the level was not affected by Na3VO4 treatment. In contrast, in incubates of EF tissue, Na3VO4 induced dosage-dependent increases in PGE and PGF at either stage. The Na3VO4-stimulated increase of PGE in preOV follicle incubates was significantly reduced by the translational inhibitor, cycloheximide (5 μM), but not by the transcriptional inhibitor, actinomycin (5 μM). PGF levels in preOV follicle incubates were also significantly reduced by cycloheximide and actinomycin in controls, but not in the presence of 0.1 mM Na3VO4. The results suggest that protein synthesis was required for Na3VO4 to increase accumulation of PGE, and in maintaining control PGF levels in preOV follicles. In addition, since PGF levels in preOV follicles were not reduced by either inhibitor in the presence of Na3VO4, a Na3VO4-stimulated increase of PGF levels was unmasked that apparently acts through a non-translational pathway. In vitro ovulation was also significantly increased by 0.1 mM Na3VO4. However, the Na3VO4-induced ovulation was not inhibited by either actinomycin or cycloheximide. The data imply that the mechanism(s) by which Na3VO4 induces ovulation are distinct from that for stimulating PG accumulation. When preOV follicles were incubated with 10 μM forskolin, no stimulatory effect on ovulation, or on PGE and PGF levels was observed. The data strongly indicate that the effects of Na3VO4 on ovulation and ovarian PG levels were not mediated by an increase in cAMP.

Paracrine interactions between platelet-activating factor and prostaglandins in hormonally-treated human luteal phase endometrium in vitro

Stromal cells and epithelial glands were separated after enzymic digestion of specimens obtained from 27 women at hysterectomy or endometrial biopsy during the luteal phase, and then cultured to confluence in vitro. PGE release into the culture medium (mean +/- s.e.m.: ng/mg protein/24 h) from gland cell cultures was not changed by oestradiol (17.6 +/- 1.3 for control and 25.5 +/- 2.8 for oestradiol, respectively). However, in the presence of oestradiol, PAF (5 ng/ml) significantly elevated PGE release to 44.2 +/- 5.8. No stimulation was observed in the presence of progesterone. Stromal cell medium had no effect on PGE release in gland cell cultures. PGE release was always much lower in stromal cell cultures than in glands (control: 4.7 +/- 0.6). PAF stimulated PGE release in the presence of oestradiol in these cells also; gland cell medium was without effect. In co-cultures of glandular and stromal cells, PGE release was more similar to that seen in gland cell cultures, with PAF being stimulatory under the influence of oestradiol. PGF release into the medium from the same gland cell cultures was significantly elevated by hormonal treatment, being greatest (62.0 +/- 11.3) with oestradiol alone, and was strongly inhibited in all wells by addition of PAF and stromal cell medium. In stromal cell cultures without hormonal addition, PGF levels (15.0 +/- 2.4) were similar to those seen in glands (18.1 +/- 3.1), and no stimulation was achieved by oestradiol (29.6 +/- 5.9). PAF was inhibitory on PGF release, while gland cell medium was without effect. Co-cultures gave PGF values generally similar to those of stromal cells; oestradiol was again stimulatory (55.0 +/- 9.3). PAF was significantly inhibitory in the presence of oestradiol. PAF (mean +/- s.e.m.: pmol/mg protein/24 h using a platelet serotonin release assay) in stromal cells was significantly increased from control [M199 alone] (0.31 +/- 0.12) by progesterone (1.00 +/- 0.17). Addition of PGE-2 (7.5 ng/ml) to progesterone-treated wells further increased PAF concentration (5.34 +/- 0.09), but was without effect in wells receiving oestradiol alone. Wells exposed to both hormones exhibited an intermediate response. Similar results were obtained with addition of gland cell culture medium, presumably due to its endogenous PGE content. In co-cultures, PAF concentrations were significantly elevated by progesterone alone (4.78 +/- 0.78) or when combined with oestradiol (2.38 +/- 0.51), but not by oestradiol alone. Treatment with PGE-2 caused no additional stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

C-reactive protein and 6-keto prostaglandin F 1-α in patients with gynecologic cancer

C-reactive protein (CRP) is an acute phase reactant that appears to have a variety of biologic effects, including stimulation of prostaglandin production by peripheral blood monocytes. Both CRP and 6-keto prostaglandin F 1-α (6-keto PGF 1-α) have been noted to be elevated in the sera of patients with malignant disease, therefore the current study was undertaken to determine whether any correlation exists between serum levels of these two substances. Thirty-five samples of sera from 16 patients undergoing treatment for primary gynecologic malignancies were tested. CRP was elevated above normal in 97% of samples and 6-keto PGF 1-α was elevated in 91% of samples. No correlation between levels of CRP and 6-keto PGF 1-α was identified. Serial serum samples were available for 6 patients undergoing therapy; in 5 of 6 patients CRP levels reflected the clinical disease course. There was no apparent correlation between 6-keto PGF 1-α levels and clinical progression or regression of disease.

The role of arachidonic acid metabolites in mediating ethanol self-administration and intoxication.

Prostaglandin synthesis inhibitors antagonize the effects of alcohols, indicating that some aspect of cyclooxygenase activity and arachidonic acid metabolism is involved in the mechanism of action of alcohols. In addition, ethanol increases in vivo brain PGE and PGF levels in a manner correlated across dose and time with the absorption phase of ethanol. These results have provided systematic evidence in support of the hypothesis that ethanol produces its intoxicating effects to a significant degree through a prostaglandin-mediated mechanism. This report has presented an overview of this work, as well as additional results from a series of recent studies that examined the effects of pretreatment with INDO, a potent PGSI, on ethanol self-administration. The results of these self-administration studies indicate that INDO can decrease responding for ethanol in a dose-related manner. The pattern of changes suggests that INDO decreases ethanol self-administration by decreasing the reinforcing effects of ethanol and not by producing a conditioned aversion to ethanol. In a subsequent study, INDO did not affect saccharin self-administration. These results suggest that there exists a common prostaglandin-related mechanism that is important in the mediation of both acute sensitivity to ethanol and the reinforcing properties of this drug. These findings may provide for the development of novel pharmaceutical treatments for acute alcohol overdose as well as for chronic alcohol abuse.

Levels of LH, progesterone and estradiol-17β during natural and PGF 2α-induced estrus in Indobrazil and Brown Swiss cows in the tropics

A comparison was made under tropical conditions between seven Indobrazil (IB) and six Brown Swiss (BS) cows with regard to the blood levels of luteinizing hormone (LH), progesterone (P 4) and estradiol-17β (E 2) during a PGF 2α-induced estrus and the natural estrus of the following cycle. After a double injection of 25 mg of PGF 2α 11 days apart, blood samples were taken every 3 h for 5 days, and this bleeding regime repeated for another 5 days starting on day 18 of the cycle that followed the second injection. Estrus occurred at 75.0 ± 6.1 and 69.4 ± 5.3 h after injection in IB and BS, respectively (NS). There was a decrease in P 4 concentration after PGF 2α and levels lower than 1.0 ng/ml were detected 24 h after the injection. The levels of P 4 decreased again at the end of the following estrous cycle from 60 to 30 h before the natural estrus in IB and BS. Estrogen concentrations were extremely variable and differences were not significant. The highest levels of E 2 were 23.7 and 24.7 pg/ml in the induced estrus and 15.2 and 25.5 pg/ml in the natural estrus of IB and BS cows, respectively; the peak value was observed on average 20 h before estrus in all groups. No significant differences between IB and BS were found in the concentration of LH, the peak occurring almost at the onset of the estrus (4.9 ± 0.6 h IB and 6.8 ± 0.6 h BS), except when the area under the LH curve was compared; here a significant effect of breed on LH concentration was found ( P < 0.05).

Ovarian prostaglandin levels at the midsequence oviposition, the terminal ovipostion and the first ovulation of a sequence in the hen (Gallus domesticus).

Prostaglandin (PG) F and E levels in plasma and tissues were examined at the midsequence oviposition (CsOP), the terminal oviposition (CtOP) and the first ovulation (C1OV) of a sequence. PG levels were determined in (1) plasma from the brachial, uterine and three largest preovulatory folliclular veins, (2) theca and granulosa layers of the five largest preovulatory and three postovulatory follicles, and (3) myometrium and mucosa layers of the uterus. PGF levels in peripheral and uterine plasma were about the same between CsOP, CtOP and C1OV. At CsOP and C1OV, plasma PGF levels in the largest preovulatory follicle (F 1) were higher than those in the second (F 2) and third largest (F 3) follicles. On the other hand, PGF level in the F 1 plasma at CtOP was not higher than that in the F 2 plasma and lower than those in the F 1 plasma at CsOP and C1OV. The amounts of PGF detected in the theca layers at CsOP and C1OV increased with follicular growth reaching a maximum in F 1. In contrast, PGF level in the F 1 theca layer at CtOP was lower than those at CsOP and C1OV. However, PGF level in the theca layer of the largest postovulatory follicle (R 1) at CtOP increased to the same level in the F 1 theca at CsOP and C1OV. PGF level in the granulosa layer did not change with follicular size increase. PGE level of theca layer was high in F 2 and F 1 at each case, whereas PGE level in the granulosa layer did not change with follicular growth. PGF levels in the myometrium and mucosa layers were about the same through the three cases examined. These results suggest that in the cases of C1OV and CsOP, processes associated with ovulation may be related to PG synthesis in F 1, while only in the case of CtOP, R 1 may provide a signal for the terminal oviposition of a sequence, because it is not accompanied by the ovulatory process.

Prostaglandin levels in plasma and follicular and uterine tissues of the quail in relation to midsequence oviposition.

Changes in the concentration of prostaglandin (PG) F and E in plasma and reproductive tissues were measured during the oviposition cycle in the quail. Tissue samples were collected from the shell gland (uterus), the three largest preovulatory follicles, and the largest postovulatory follicle (R1). Plasma and tissue samples were collected 16 and 8hr before and immediately after a midsequence oviposition. Plasma PGF and PGE concentrations showed a 2-fold increase at oviposition (P<0.05). PGF concentrations in the preovulatory follicles remained stable, but the PGF level in R1 at oviposition significantly increased (P<0.05). Follicular PGE concentrations were not different from preceding point value. There were no changes in PGF and PGE concentrations of the uterine tissue throughout the oviposition cycle. These results suggest that the increases in plasma PGF and PGE levels may play a role in the regulation of oviposition in the quail and the ovarian follicle may be the origin of the increased plasma PGs at oviposition.

Interrelationship between arginine vasotocin, prostaglandin, and uterine contractility in the control of oviposition in the hen ( Gallus domesticus)

Uterine electromyographic activity (EMG), plasma concentrations of prostaglandin (PG) F and E, and arginine vasotocin (AVT) were simultaneously measured in relation to PGE 2-induced premature oviposition and to indomethacin-blocked oviposition in chickens. The administration of indomethacin (5 mg, im) 3 hr before the predicted time of oviposition delayed egg lay by 8–14 hr, whereas control hens laid eggs at the predicted time. In indomethacin-treated hens increases in uterine EMG activity and plasma concentrations of PGF, PGE, and AVT were not observed at the expected time of oviposition, whereas a marked increase in plasma PGF and AVT occurred during spontaneous oviposition. The intrauterine administration of PGE 2 (1 μg) 3 hr before predicted oviposition induced premature egg lay within 5 min. Premature oviposition was accompanied by significant elevations in both uterine EMG activity and plasma levels of AVT. Changes in plasma levels of PGF and PGE were not observed. When premature oviposition was induced, significant increases in EMG activity and plasma concentrations of PGF and AVT were observed at the expected time of oviposition in the absence of an egg in the uterus. The administration of PGE 2 at the predicted time of oviposition in hens pretreated with indomethacin induced oviposition which was accompanied by a significant increase in plasma AVT levels. The results suggest that AVT release is stimulated by uterine contractility in chickens.

Amniotic fluid prostaglandins F 2α and E 2 , measured at artificial rupture of the membranes”, predict the subsequent progress of labour

Prostaglandin F 2α and E 2 concentrations in the amniotic fluid and fetal membranes of 35 patients was analysed, in order to investigate differences in prostaglandin synthesis in parous and nulliparous women, and to find whether women who subsequently required oxytocin to accelerate labour, showed any difference in intrauterine prostaglandin concentrations. Significantly less PGF 2α was detected in the amniotic fluid of women who required oxytocin, and fetal membrane PGE 2 was significantly lower in these women at delivery. Differences in PGE 2 and PGF 2α in parous and nulliparous women were less mar ed. Amniotic fluid levels of PGF 2 at Artificial Rupture of the Membranes (ARM), and the ratio of PGF 2α/PGE 2 at ARM, were prognostic for the subsequent progression of labour.

Time course of ethanol's effects on brain prostaglandins in LS and SS mice

Prostaglandin synthesis inhibitors antagonize behavioral responses to alcohols. Recent work has shown that ethanol increases brain prostaglandin (PG) levels. The study reported here examined the tine course for ethanol-stimulated brain PGE and PGF production in Long Sleep and Short Sleep mice, animals bred selectively for high vs. low acute response to ethanol. Increases in brain PGE levels correlated highly with the absorption phase but only partially with the elimination phase of ethanol. PGF levels correlated significantly with blood ethanol levels across the entire three hour period. These results, plus sex and genotype interactions, provide further evidence to support the hypothesis that ethanol produces its intoxicating effects to a significant degree through a prostaglandin mediated mechanism.

Effect of time and dose of indomethacin on follicular prostaglandins and ovulation in the rabbit.

This study determined specifically when ovarian prostaglandins (PGs) increase during ovulation and how effectively different doses of indomethacin inhibit PGs and ovulation. Rabbit ovarian follicles were removed at hourly intervals after stimulating the animals with hCG (50 IU/kg). The follicles were homogenized in 0.1 M acetate buffer (pH 4.5), and the PGE and PGF in the extracts were measured by RIA. Ovulation rates were determined by calculating the percentage of mature follicles that ruptured after stimulation by hCG. Before hCG, the normal levels of PGE and PGF were 111.1 +/- 14.7 and 51.0 +/- 6.6 pg/mg follicle, respectively. By 2 h after hCG treatment, PGE and PGF both increased to 162.6 +/- 17.0 and 80.6 +/- 13.3 pg/mg follicle, respectively. Approximately 5 h later, there was a second, sharper increase in both PGs which peaked at 652.6 +/- 63.5 and 345.4 +/- 32.3 pg/mg follicle, respectively, 10 h after hCG treatment, i.e. at the expected time of ovulation. We found that regardless of whether indomethacin was given early or late during the ovulation process, this agent significantly reduced follicular PG production within 5 min after its administration. For example, only 5 min after 10 mg/kg indomethacin were administered 8 h after hCG, PGE and PGF dropped from 317.7 +/- 50.0 and 125.0 +/- 10.5 pg/mg follicle to 93.3 +/- 17.4 and 49.3 +/- 10.5 pg/mg follicle, respectively. Unexpectedly, when graded doses of indomethacin were administered either 1 or 8 h after hCG, there was not a statistically significant correlation between follicular PG levels and ovulation rate. For example, when doses of 1.25, 2.5, 5.0, and 10.0 mg/kg indomethacin were given 8 h after hCG, the PGE and PGF levels at the expected time of ovulation (i.e. 2 h later) were always equal to or less than the PG levels in follicles that had not been stimulated by hCG, yet ovulation proceeded at rates of 46.7 +/- 12.3%, 30 +/- 7.7%, 14.3 +/- 9.3%, and 0%, respectively. Therefore, the results raise questions about the specific role of PGs in the ovulation process.

Investigations on the control of in vitro spontaneous brook trout ( Salvelinus fontinalis) ovulation

The possible roles of follicular cyclooxygenase and cAMP in the control of in vitro spontaneous brook trout ( Salvelinus fontinalis) ovulation were investigated. Brook trout oocytes that had undergone germinal vesicle breakdown and follicular separation in vivo, were incubated in vitro in the presence of indomethacin. At 3 or 30 μM, indomethacin significantly reduced the levels of PGF and PGE (measured by radioimmunoassay) in the incubation medium but did not inhibit spontaneous ovulation in vitro. Follicular cAMP levels were measured by a competitive protein binding assay, prior to and during spontaneous ovulation. cAMP levels were approximately 3.2 pmol/mg protein prior to incubation and did not fluctuate significantly from this value throughout the 24-hr incubation period. The phosphodiesterase inhibitor, 3-isobutyl-1-methyl-xanthine, significantly increased follicular cAMP levels at 1.0 and 0.1 m M. The combined results suggest that cyclooxygenase metabolites or a decrease in cAMP are not involved in the control of spontaneous brook trout ovulation in vitro. The in vitro effects of primaquine, a putative phospholipase mediator, were also investigated. At lower concentrations (0.1 – 0.5 m M), primaquine significantly enhanced ovulation above that observed in spontaneous controls. However, at 1.0 m M, primaquine inhibited spontaneous ovulation. Indomethacin at 3 or 30 μ M did not block the stimulatory effect of primaquine observed at lower concentrations, indicating that cyclooxygenase metabolites are not involved in the stimulatory effect of primaquine on ovulation.