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At least 19 recordsLinked to original sources
PubMed1979

Metabolism of prostaglandin E1 and of glutathione conjugate of prostaglandin A1 (GSH-prostaglandin A1) by prostaglandin 9-ketoreductase from rabbit kidney.

Rabbit kidney prostaglandin 9-ketoreductase was found to metabolize the glutathione conjugate of prostaglandin A1 (GSH-prostaglandin A1). Apparent Km (GSH-prostaglandin A1) 13 microM and apparent Km (prostaglandin E1) 200 microM. The cytosolic preparation was subjected to gelfiltration and isoelectric focusing, which revealed that metabolism of prostaglandin E1 and GSH-prostaglandin A1 occurs by means of the same fractions. Furthermore, prostaglandin E1 and GSH-prostaglandin A1 are competitive inhibitors of the enzyme, when GSH-prostaglandin A1 and prostaglandin E1 are tested as substrates, respectively. It si concluded, that GSH-prostaglandin A1 is a much better substrate for prostaglandin 9-ketoreductase from rabbit kidney than is prostaglandin E1.

Animals↗
PubMed1986

Stereospecific conversion of prostaglandin D2 to (5Z,13E)-(15S)-9 alpha-11 beta,15-trihydroxyprosta-5,13-dien-1-oic acid (9 alpha,11 beta-prostaglandin F2) and of prostaglandin H2 to prostaglandin F2 alpha by bovine lung prostaglandin F synthase.

A prostaglandin F (PGF) synthase was recently purified from bovine lung that catalyzed the reduction of both PGH2 and PGD2 but at different active sites on the enzyme. In view of the recent finding that PGD2 is stereospecifically reduced to a unique biologically active compound, (5Z, 13E)-(15S)-9 alpha, 11 beta, 15-trihydroxyprosta-5,13-dien-1-oic acid (9 alpha,11 beta-PGF2 or 11-epi-PGF2 alpha), by a human liver cytosolic enzyme, detailed characterization of the products formed from PGH2 and PGD2 by the bovine lung PGF synthase was carried out. Chromatographic characteristics of the products formed and stereochemical analysis procedures using mass spectrometry indicated that the enzyme stereospecifically reduces PGH2 to PGF2 alpha, whereas PGD2 is stereospecifically converted to 9 alpha,11 beta-PGF2. The finding that this enzyme catalyzes the formation of both C-11 hydroxy epimers of PGF2, albeit from different substrates, is of interest in that these two compounds may exert different biological actions.

Animals↗
PubMed1987

Estrogen, progesterone, prolactin, prostaglandin E2, prostaglandin F2 alpha, 13,14-dihydro-15-keto-prostaglandin F2 alpha, and 6-keto-prostaglandin F1 alpha gradients across the uterus in women in labor and not in labor.

Before or during labor in humans, changes in peripheral levels of estrogen and progesterone are not evident. Local alterations of estrogen, progesterone, and prolactin concentrations may be present and be accompanied by prostaglandin changes. The purpose of this study was to investigate the differences in concentrations of these hormones across the uterus and to evaluate their interrelationships in patients at term gestation with and without labor. Blood samples were obtained from a radial artery and a uterine vein in 22 women without and in 10 with labor. The difference between levels in the two blood vessels was designated as the gradient. Neither levels nor gradients were different between the two groups for estrone, estradiol, estriol, progesterone, or prolactin. The plasma levels of prostaglandin F2 alpha, 13,14-dihydro-15-keto-prostaglandin F2 alpha, and prostaglandin E2 were significantly increased in labor. Prostacyclin levels, as indicated by the 6-keto-prostaglandin F1 alpha metabolite, were not altered. The gradients for prostaglandin F2 alpha and E2 were significantly increased in labor. The results of the study also suggested that, in gestation at term, serum prolactin is produced mainly by the pituitary and that estrone may originate from peripheral conversion of estradiol. We conclude that in humans prostaglandin gradients of the E and F groups are increased in labor. These increases are not associated with changes in sex steroids or prolactin. Prostacyclin metabolite gradients also appear not to be altered in labor, suggesting that some prostaglandins are selectively increased in early labor either by enhanced production or decreased metabolism or both.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

The use of immobilized ligands and [125I]protein a for immunoassays of thromboxane B2, prostaglandin D2, 13,14-dihydro-prostaglandin E2, 5,6-dihydro-prostaglandin I2, 6-keto-prostaglandin F1 alpha, 15-hydroxy-9 alpha, 11 alpha(epoxymethano)prosta-5,13-dienoic acid and 15-hydroxy-11 alpha,9 alpha(epoxymethano)prosta-5,13-dienoic acid.

Immunoassays were developed for quantitative determination of thromboxane B2, prostaglandin D2, 13,14-dihydro-prostaglandin E2, 5,6-dihydro-prostaglandin I2, 6-keto-prostaglandin F1 alpha, 15-hydroxy-9 alpha, 11 alpha (epoxymethano) prosta-5, 13-dienoic acid and 15-hydroxy-11 alpha, 9 alpha (epoxymethano) prosta-5,13-dienoic acid. Ligands immobilized by covalent linkage to a solid support, bound homologous rabbit antibodies. [125I] Protein A was used to measure the bound IgG antibody. Increments of homologous and heterologous fluid-phase ligand completed with solid-phase ligand for antibody and resulted in decreasing amounts of bound [125I]-Protein A. The serologic specificity for each immune system was determined. Immunoassays for thromboxane B2, 6-keto-prostaglandin F1 alpha, and 5,6-dihydro-prostaglandin I2 were used to identify their respective homologous ligands that were separated by normal phase and reversed phase high pressure liquid chromatography.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Prostaglandins for prevention of postpartum haemorrhage.

BACKGROUND: Prostaglandins have mainly been used for postpartum haemorrhage when other measures fail. Misoprostol, a newer and cheaper prostaglandin E1 analogue, has sometimes been used for management of the third stage of labour. OBJECTIVES: The objective of this review was to assess the effects of prophylactic prostaglandin use in the third stage of labour. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register were searched. Researchers in the field were also contacted. Date of the latest search: December 1999. SELECTION CRITERIA: Randomized or quasi-randomized trials comparing a prostaglandin agent with another uterotonic or no prophylactic uterotonic (nothing or placebo) as part of management of the third stage of labour. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality was assessed by one reviewer. MAIN RESULTS: Seven trials were included. There were six trials of injectable prostaglandins and one of rectal misoprostol. The main limitations of these studies are their small sample sizes and lack of blind assessment of the outcomes. Injectable prostaglandins were associated with decreased blood loss (weighted mean difference -72 millilitres, 95% confidence interval -70 to -75) and shortened duration of third stage when compared to other uterotonics. Severe postpartum haemorrhage (1000 millilitres or more blood loss) occurred in two of four studies and was seen in fewer women receiving prostaglandins, though the difference was not statistically significant. Adverse effects (vomiting, diarrhoea and abdominal pain) were more common with prostaglandins when compared to other uterotonic agents. REVIEWER'S CONCLUSIONS: Although injectable prostaglandins appear to be effective in preventing postpartum haemorrhage, concerns about safety and costs limit their suitability for routine prophylactic management of third stage of labour. However, injectable prostaglandins should continue to be used for the treatment of postpartum haemorrhage when other measures fail. Misoprostol is cheap, stable and seems to be safe. Trials addressing the effectiveness of misoprostol are continuing.

Female↗
PubMed1977

Prostaglandins and abortion. III. Comparison of single intra-amniotic injections of 15-methyl prostaglandin F2alpha and prostaglandin F2alpha for termination of second-trimester pregnancy: an international multicenter study. World Health Organization Tast Force on the Use of Prostaglandins forthe Regulation of Fertility.

A multicenter, multinational study involving 1,521 patients has compared prostaglandin F2alpha (PGF2alpha) (40 or 50 mg.) and 15-methyl PGF2alpha (2.5 mg.) given intra-amniotically for induction of second-trimester abortion. The highest success rates for PGF2alpha at 24 and 48 hours were 67.8 and 86.6 per cent, respectively. The percentages for 15-methyl PGF2alpha for the equivalent times were 74.1 and 95.6 per cent, respectively. There were 75 cases classified as failures in 602 patients treated with PGF2alpha and only 34 cases were classified as failures among 919 patients treated with 15-methyl PGF2alpha. A further 35 patients required additional treatment to complete the abortion. The over-all incidence of diarrhea and vomiting was low, less than 3.4 episodes per patient. There were 20 cases of cervical laceration (2.9 per cent); only one extended into the lower segment of the uterus. It is concluded that intra-amniotic administration of either 50 mg. of PGF2alpha or 2.5 mg. 15-methyl PGF2alpha provides an effective and safe method for termination of second-trimester pregnancies.

Abortion, Induced↗
PubMed1993

Prostaglandin D2 and endothelin-1 induce the production of prostaglandin F2 alpha, 9 alpha, 11 beta-prostaglandin F2, prostaglandin E2, and thromboxane in capillary endothelium of human brain.

Endothelial cells derived from human brain capillaries (HBCEC) synthesize prostaglandin D2 (PGD2) which can be stimulated, among other prostanoids, by endothelin 1 (ET-1). Both the PGD2 induced by ET-1 and the exogenously added PGD2 to HBCEC are converted to 9 alpha, 11 beta-prostaglandin F2 (9 alpha, 11 beta-PGF2), a known potent vasoconstrictor. Exogenous PGD2 also dose-dependently enhanced the production of vasoconstrictive PGF2 alpha, thromboxane B2 (TXB2), and the vasodilatory PGE2 as well as cAMP by HBCEC. The PGD2-induced formation of PGF2 alpha, PGE2, and TXB2 was reduced by the cyclooxygenase inhibitors acetylsalicylic acid (ASA) or indomethacin (Indo), indicating for the first time that PGD2 may contribute to the formation of prostanoids in HBCEC. These results strongly suggest that PGD2 may play an important role in the regulation of cerebral capillary function under physiologic and pathologic conditions.

1-Methyl-3-isobutylxanthine↗
PubMed1985

Enzymatic formation of prostaglandin F2 alpha from prostaglandin H2 and D2. Purification and properties of prostaglandin F synthetase from bovine lung.

Prostaglandin F synthetase from bovine lung was purified 540-fold to apparent homogeneity, as assessed by polyacrylamide gel electrophoreses and ultracentrifugation. The purified enzyme proved to be a monomeric protein with a molecular weight of about 30,500. The enzyme catalyzed not only the reduction of the 11-keto group of prostaglandin D2 but also the reduction of 9,11-endoperoxide of prostaglandin H2 and various carbonyl compounds (e.g. phenanthrenequinone). Experiments using column chromatography, polyacrylamide gel electrophoreses, immunotitration using antibody against the purified enzyme, and heat treatment indicated that three enzyme activities resided in a single protein. Although phenanthrenequinone and prostaglandin D2 competitively inhibited the prostaglandin D2 and phenanthrenequinone reductase activities, respectively, these two substrates were all but ineffective on the prostaglandin H2 (at the Km value) reductase activity up to 14-fold of those Km values. These results suggest that a single enzyme protein purified from the bovine lung catalyzes the reduction of prostaglandin D2, prostaglandin H2, and various carbonyl compounds and that prostaglandin D2 and prostaglandin H2 are metabolized at two different active sites, yielding prostaglandin F2 alpha as the reaction product.

Amino Acids↗
PubMed1987

Metabolism of prostaglandin D2 in isolated rat lung: the stereospecific formation of 9 alpha,11 beta-prostaglandin F2 from prostaglandin D2.

The metabolic transformation of exogenous prostaglandin D2 was investigated in isolated perfused rat lung. Dose-dependent formation (2-150 ng) of 9 alpha,11 beta-prostaglandin F2, corresponding to about 0.1% of the perfused dose of prostaglandin D2, was observed by specific radioimmunoassay both in the perfusate and in lung tissue after a 5-min perfusion. To investigate the reason for this low conversion ratio, we analyzed the metabolites of tritium-labeled 9 alpha,11 beta-prostaglandin F2 and prostaglandin D2 by boric acid-impregnated TLC and HPLC. By 5 min after the start of perfusion, 9 alpha,11 beta-prostaglandin F2 disappeared completely from the perfusate and the major product formed remained unchanged during the remainder of the 30-min perfusion. The major product was separated by TLC and identified as 13,14-dihydro-15-keto-9 alpha,11 beta-prostaglandin F2 by GC/MS. In contrast, pulmonary breakdown of prostaglandin D2 was slow and two major metabolites in the perfusate increased with time, each representing 56% and 11% of the total radioactivity at the end of the perfusion. The major product (56%) was identified as 13,14-dihydro-15-ketoprostaglandin D2 and the minor one (11%) was tentatively identified as 13,14-dihydro-15-keto-9 alpha,11 beta-prostaglandin F2 based on the results from radioimmunoassays, TLC, HPLC, and the time course of pulmonary breakdown. These results demonstrate that the metabolism of prostaglandin D2 in rat lung involves at least two pathways, one by 15-hydroxyprostaglandin dehydrogenase and the other by 11-ketoreductase, and that the 9 alpha,11 beta-prostaglandin F2 formed is rapidly metabolized to 13,14-dihydro-15-keto-9 alpha,11 beta-prostaglandin F2.

Animals↗
PubMed1981

Prostaglandins and steroidogenesis in isolated bovine adrenal cells. Effects of ACTH, prostaglandin-synthesis inhibitors, prostaglandins and prostaglandin analogs.

In bovine adrenal cortex cells, dispersed without preferential loss of cells, we investigated (1) whether endogenous prostaglandins (PGs) are involved in ACTH-induced adrenal steroidogenesis, and (2) the steroidogenic effects of PGs and PG analogs. Free cells produced considerable amounts of PGE2, whereas only minute quantities of PGF2 alpha and PGA1 were synthesized. PGE2 synthesis, however, was not significantly increased when ACTH elicited a steroidogenic response in free cells. High concentrations of PG-synthesis inhibitors such as indomethacin affected both PG synthesis and steroidogenesis, whereas intermediate concentrations (10(-6) M) inhibited production of both PGE2 and aldosterone even after cAMP and cortisol response to ACTH had returned to normal values. It is concluded that endogenous PGE2 is not a link in the acute mechanism of action of trophic hormones in which cAMP is involved. Of the prostanoid structures, PGs of the E series were the most potent stimulating agents of cortisol production, although less active than ACTH. On the other hand, PGA1 induced an ACTH-like aldosterone synthesis. PGE2 was less active, and other prostanoid structures were without effect on aldosterone production. It is suggested that in pathological circumstances, PGA1 regulates aldosterone production and PGE2 increases both aldosterone and cortisol production.

Adrenal Cortex↗
PubMed1998

Pharmacology of [3H]prostaglandin E1/[3H]prostaglandin E2 and [3H]prostaglandin F2alpha binding to EP3 and FP prostaglandin receptor binding sites in bovine corpus luteum: characterization and correlation with functional data.

Specific binding of [3H]prostaglandin (PG) E1, [3H]PGE2 and [3H]PGF2alpha to washed total particulate homogenates of bovine corpus luteum comprised 60 to 82% of total binding. Scatchard analysis of competition data revealed the presence of an apparent single population of binding sites for [3H]PGE1 and [3H]PGE2 with dissociation constants (Kds) of 2.76 to 3.39 nM and apparent receptor density (Bmax) of 1.5 to 1.56 pmol/g wet weight (n = 3-4). However, [3H]PGF2alpha appeared to interact with two classes/states of binding sites (Kd1 = 6.51 +/- 0.65 nM, Bmax1 = 2.33 +/- 0.26 pmol/g wet weight; Kd2 = 986 +/- 269 nM; Bmax2 = 44.8 +/- 11.3 pmol/g wet weight, n = 11). Specific [3H]PGE1 and [3H]PGE2 binding was most potently (nanomolar affinity) inhibited by PGs with high selectivity for the EP3 receptor subtype (e.g., GR63799, sulprostone, enprostil) but was weakly (Kis > 1 microM) influenced by EP1-selective (SC-19220), FP-selective (fluprostenol, PHXA85), DP-selective (BWA868C; ZK118182), IP-selective (iloprost) and TP-selective (U46619) PGs. Specific [3H]PGF2alpha binding was potently displaced by FP-selective agents such as fluprostenol, PHXA85 and cloprostenol with nanomolar affinities (n = 3-25), but weakly (Kis > 1 microM) by other PGs showing high selectivity for other PG receptor subtypes mentioned above. The relative specificities and potencies of EP3- and FP-selective PGs tested in the binding assays were confirmed using various functional assays. These studies have provided strong pharmacological evidence for the similarity of [3H]PGE1 and [3H]PGE2 binding to EP3 receptors and for [3H]PGF2alpha binding to FP receptors in washed bovine corpus luteum homogenates.

Alprostadil↗
PubMed1985

The effects of alpha- and beta-adrenergic stimulation on contractility and prostaglandin (prostaglandins E2 and F2 alpha and 6-keto-prostaglandin F1 alpha) production of pregnant human myometrial strips.

The effects of catecholamines and alpha- and beta-adrenergic agonists and antagonists on the spontaneous contractility of superfused pregnant human myometrial strips are reported. Prostaglandins (prostaglandins E2 and F2 alpha and 6-keto-prostaglandin F1 alpha) were analyzed in the effluent of the superfusion medium by specific radioimmunoassays. Both epinephrine and norepinephrine dose-dependently (10 ng/ml to 1 microgram/ml) stimulated the contractility of the myometrial strips and significantly increased the synthesis of all prostaglandins assayed. alpha-Adrenergic blockers inhibited the catecholamine-induced increase in contractility. This was associated with decreased prostaglandins F2 alpha and E2 concentrations and a further increase in 6-keto-prostaglandin F1 alpha levels. Exclusive beta-adrenergic stimulation with beta-mimetic drugs had the same effect. Conversely, epinephrine stimulation together with beta-blockers resulted in a further increase in the prostaglandins F2 alpha and E2 release of the myometrial strips. This effect was even more pronounced with specific alpha-adrenergic stimulant drugs. Our results demonstrate the interrelationship of alpha- and beta-adrenergic stimulation and the prostaglandin system. alpha-Adrenergic stimulation increases myometrial contractility and the synthesis of prostaglandins F2 alpha and E2. beta-Adrenergic stimulation reduces contractility by further enhancing 6-keto-prostaglandin F1 alpha production.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Lack of specific binding of prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha to serum in patients with peptic ulcer disease and in healthy subjects.

Rabbits immunized against prostaglandins develop antibodies to prostaglandins and peptic ulcer disease (duodenal and gastric ulcers). We have evaluated the hypothesis that idiopathic gastric or duodenal ulcer disease in humans may be associated with the spontaneous occurrence of serum antibodies directed against endogenous prostaglandins. We found that serum from 45 ulcer patients (34 duodenal, 11 gastric) had a low degree of binding of radiolabeled prostaglandin E2, prostaglandin F2 alpha, or 6-keto prostaglandin F1 alpha. The extent to which prostaglandins were bound to serum of ulcer patients was not statistically different from prostaglandin binding to serum from 25 normal subjects. Therefore, we conclude that spontaneous occurrence of circulating antibodies against endogenous prostaglandins is an unlikely cause of gastroduodenal ulceration in humans.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

9 alpha,11 beta-prostaglandin F2 formation in various bovine tissues. Different isozymes of prostaglandin D2 11-ketoreductase, contribution of prostaglandin F synthetase and its cellular localization.

9 alpha,11 beta-prostaglandin F2 was formed from prostaglandin D2 by its 11-ketoreductases in 100,000 x g supernatants of various bovine tissues in the presence of an NADPH-generating system. The reductase activities were high in liver (51.09 nmol/h/mg of protein), lung (24.99), and spleen (14.20); moderate in heart and pancreas (3.09-3.61); weak in stomach, intestine, colon, kidney, uterus, adrenal gland, and thymus (0.11-2.63); and undetectable in brain, retina, carotid artery, and blood (less than 0.10). No formation of prostaglandin F2 alpha from prostaglandin D2 was detected in all tissues. In immunotitration analyses with a polyclonal antibody specific for prostaglandin F synthetase, the reductase activities in lung and spleen showed identical titration curves to that of the purified synthetase and decreased to less than 15% of the initial activity under the condition of antibody excess. Prostaglandin F synthetase-immunoreactive protein in these two tissues showed peptide fingerprints identical to that of the purified enzyme after partial digestion with Staphylococcus aureus V8 protease. The antibody was partially cross-reactive to the reductase in liver (about 20% of that to the synthetase) but not to the reductase(s) in other tissues. The Km value for prostaglandin D2 of the reductase activity was the same in lung and spleen as that of the purified prostaglandin F synthetase (120 microM) but differed in liver (6 microM), heart, and pancreas (15 microM). The predominant distribution of prostaglandin F synthetase in lung and spleen was confirmed by radioimmunoassay (2.8 and 1.0 micrograms/mg protein, respectively) and Northern blot analyses. In immunoperoxidase staining, this enzyme was localized in alveolar interstitial cells and nonciliated epithelial cells in lung, histiocytes and/or dendritic cells in spleen, and a few interstitial cells in kidney and adrenal cortex.

Animals↗
PubMed1986

GnRH effects on placental hormones during gestation. III. Prostaglandin E, prostaglandin F, and 13,14-dihydro-15-keto-prostaglandin F.

We studied the release of prostaglandin E (PGE), prostaglandin F (PGF) and 13,14-dihydro-15-keto-prostaglandin F (MPF) from explants of human placentas of different gestational ages and the effect of gonadotropin-releasing hormone (GnRH) on this release. The greatest basal release of PGE, PGF and MPF was in the cultures from 9- to 13-wk placentas, with the release on the second and third days of culture increasing 4- to 10-fold from that of the first day. In cultures from 15-wk to term placentas, the initial basal release (Day 1) of these prostaglandins was only slightly higher than in cultures from 6-wk placentas. In cultures from term placentas, the later increase with extended culture was absent or very small. Addition of synthetic GnRH to the cultures from 6- to 9-wk placentas effected no significant change in release of PGE, PGF or MPF. However, GnRH added to the cultures from 13-wk placentas effected a dose-related inhibition of these prostaglandins. After 15 wk, we observed a stimulation of these prostaglandins by GnRH that was as much as 50-fold; stimulation was highly significant in the cultures from 16- and 17-wk, as well as in those from the term placentas. These data demonstrate an action of GnRH on prostaglandin release and indicate that both the basal release of PGE, PGF and MPF and the response to GnRH are related to the gestational age of the placenta.

Dinoprost↗
PubMed1989

Effect of acute ethanol ingestion on human gastric luminal prostaglandin E2, prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha.

In healthy human volunteers we evaluated the effect of a single oral dose of 1 g/kg of alcohol (12.5%, v/v) on the output of prostaglandin E2, prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha in the gastric juice. In control experiments performed at intervals of 5-8 days, the subjects received the identical volume of water. Ninety minutes after the ingestion of alcohol, or water, first the basal secretion and subsequently the secretion after injection of pentagastrin (6 micrograms/kg, i.m.) were collected over periods of 60 min. The concentrations of the three prostaglandins were determined by radio-immunoassay. After ingestion of alcohol, the volume of gastric juice in response to pentagastrin stimulation was reduced by 24.6%, as compared with the control period. Ingestion of alcohol led to a significant reduction in the concentration of prostaglandin E2 (-42.7%) after stimulation with pentagastrin. The prostaglandin E2 output per hour was markedly inhibited by the ingestion of alcohol, both in the basal period (-47%) and after stimulation with pentagastrin (-55%). While stimulation with pentagastrin did not influence the secretion of PGE2 or PGF2 alpha, the output of 6-keto-PGF1 alpha increased appreciably (+88%) after the administration of pentagastrin. Alcohol also significantly (-28%) inhibited the secretion of 6-keto-PGF1 alpha in the period following the administration of pentagastrin. It is supposed that the inhibition of the secretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha by acute alcohol ingestion, might be of significance for the development of alcohol-induced mucosal damage in the stomach.

6-Ketoprostaglandin F1 alpha↗