Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inactivation of prostaglandins in the placenta was studied using an assay for 15-hydroxy-prostaglandin dehydrogenase (PGDH). Forty-four patients with normal single pregnancies between 38 and 42 weeks gestation were studied. Placentae were obtained before the onset of labour in 9, after spontaneous labour in 18, and after oxytocin-induced labour in 17 cases, PGDH-activity ranged from 54 to 495 nanomoles PGF2alpha/g placenta/minute, with a mean +/- SEM of 207 +/- 18 nanomoles/g/minute. The results indicate that the PGDH content of the human placenta does not change markedly with the onset or during the process of labour. The length of either spontaneous or oxytocin-induced labour was not influenced by the PGDH content of the placenta.
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PMID:Prostaglandin dehydrogenase in the placenta before and after the onset of labour. 103 17

The metabolism of prostaglandin E2 (PGE2) was investigated in the fetal circulation of one cotyledon or a group of cotyledons in human term placentas by in vitro perfusion technique. When 100 nmol of 14C-PGE2 was infused in 2.5 minutes into the chorionic artery, 75 +/- 5% (mean +/- SEM, n=8) of the infused radioactivity appeared in the nonrecirculating venous effluent in six minutes. Most of the radioactivity was in the fraction of unmetabolized PGE2, only 6-13% of the radioactivity in the effluent appeared in metabolite fraction, the major metabolite being 14-keto-13,14-dihydro-PGE2. The amount of metabolites in 0-6 min effluent was 0.13 +/- 0.01 nmol/g of perfused placenta. This rate of formation of PGE2 metabolites is very low compared to the activity of NAD+-dependent 15-hydroxyprostaglandin dehydrogenase, which was 183 +/- 19 nmol x min-1 x g of tissue-1 (n=5) when measured from the 100.000 g supernatant fraction of homogenized human placenta using 14C-PGE2 as the substrate. The present study indicates that PGE2 is only slightly metabolized in the fetal circulation of human placenta, in spite of high activity of 15-hydroxyprostaglandin dehydrogenase in placental tissue.
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PMID:Prostaglandin E2 is only slightly metabolized in the fetal circulation of perfused human placenta. 695 52

The metabolism of prostaglandin E2 (PGE2) was decreased in isolated male hamster lungs, when sulfinpyrazone was infused into the pulmonary circulation. After pulmonary injection of 20 nmol of 14C-PGE2 the amount of 15-keto-metabolites of PGE2 was in the effluent from control lungs 4.0 +/- 0.5 nmol (mean +/- SEM) and in those from 20 mu M and 100 mu M sulfinpyrazone treated lungs 1.9 +/- 0.2 nmol (2P Less Than 0.01 compared to the control) and 1.7 +/- 0.4 nmol (2P Less Than 0.01), respectively. The amount of unmetabolized PGE2 was correspondingly increased in the effluent by sulfinpyrazone. The rate of efflux of the radioactivity from the lungs was increased by sulfinpyrazone. After injection of 10 nmol of 14C-PGE2 into the pulmonary circulation half of the injected radioactivity appeared in the effluent in 30 +/- 4 sec in control and in 15 +/- 0.7 sec (2P Less Than 0.01) in 20 mu M sulfinpyrazone experiments. Sulfinpyrazone had no effect on the activity of 15-hydroxyprostaglandin dehydrogenase in the 100.000 g supernatant fraction of homogenized hamster lungs. Thus the decreased metabolism of PGE2 in the pulmonary circulation of hamster lungs is obviously not due to the inhibition of 15-hydroxyprostaglandin dehydrogenase. A more likely explanation seems to be the decreased uptake of PGE2 into the lung cells.
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PMID:The metabolism of prostaglandin E2 is decreased by sulfinpyrazone in isolated hamster lungs. 728 Jan 18

This investigation was conducted to evaluate the potential capacity of the human fetal membranes-decidua parietalis, and in particular the chorion laeve, to degrade uterotonins that are produced in amnion, are present in amniotic fluid, or both. The four uterotonins that have been evaluated most frequently as myometrial contractants potentially involved in the initiation of human parturition are prostaglandins, oxytocin, endothelin-1, and platelet-activating factor. We assessed the levels of mRNA and the specific activities (SAs) of enkephalinase (the plasma membrane endopeptidase that degrades endothelins) and prostaglandin dehydrogenase (PGDH) in human fetal membranes, i.e. amnion and chorion leave, and in decidua parietalis. The SA of oxytocinase (which inactivates oxytocin) in these tissues also was determined. The SA of enkephalinase in chorion laeve from all anatomical sites (singleton and diamnionic-dichorionic twin placentae) in all pregnancies studied (mean +/- SEM, 95 +/- 7.9 ng/min.mg protein; n = 28) is similar to that in human fetal kidney (89.5 +/- 2.8; n = 6). Kidney tissue is believed to be one of the richest sources of enkephalinase. The SAs of enkephalinase in amnion (18.3 +/- 2.3 nmol/min.mg protein; n = 29) and in decidua parietalis (31.8 +/- 6.7; n = 20) also were high, but significantly less than that in chorion leave. The level of enkephalinase mRNA in chorion laeve in singleton pregnancies is high, as is the SA of enkephalinase (111.9 +/- 10.6 nmol/min.mg protein; n = 17). In paired chorion laeve tissues from five diamnionic-dichorionic twin placentae, the SAs of enkephalinase in reflected chorion laeve (74 +/- 12.8; P < 0.06 compared with singletons) and fused chorion laeve (64.8 +/- 6.5; P < 0.001 compared with singletons) were similar. The SA of PGDH in reflected chorion leave (46.3 +/- 6.9 nmol/min.mg protein; n = 19) was significantly greater than that in decidua (16 +/- 5.5; n = 15). There was a significant correlation between the levels of PGDH mRNA and PGDH enzyme SA. In fused chorion laeve of diamnionic-dichorionic twin placentae, the SA of PGDH (14.9 +/- 7.3; n = 4) was much less than that in reflected chorion laeve of the same twin pregnancy (70.5 +/- 14.7; n = 4). PGDH mRNA was not detectable in amnion tissue (n = 5) by northern analysis, and the SA of PGDH (< 1.2 +/- 1.0; n = 6) in amnion was undetectable or near the lower limit of assay detection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human fetal membrane contribution to the prevention of parturition: uterotonin degradation. 810 36