Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: EC:3.1.4.3 (
phospholipase C
)
18,461
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To clarify the possible mechanisms regulating prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) synthesis, the effects of gonadotropin-releasing hormone (GnRH) and substance P (SP) on the release of these two prostaglandins were studied in the oocytes of the crested newt, Triturus carnifex. Full-grown oocytes of T. carnifex, freed from follicular cells, were incubated in the presence of GnRH or SP and of the inhibitors of several enzymes involved in the release of arachidonic acid (AA) and in the conversion of AA into PGE2 and PGF2 alpha. In parallel, the same experiments were performed on oocytes with membrane phospholipids labelled with [3H]AA. In addition, the
PGE2-9-ketoreductase
activity was evaluated through the conversion of [3H]PGE2 into [3H]PGF2 alpha. The results showed that GnRH and SP could regulate prostaglandin synthesis through the activation of
phospholipase C
and diacylglycerol lipase, and through the modulation of
PGE2-9-ketoreductase
in the oocytes of T. carnifex. In particular, GnRH enhances the activity of
PGE2-9-ketoreductase
with a consequent increase in PGF2 alpha, while SP inhibits the enzyme which leads to an increase in PGE2. A similar mechanism could also be hypothesized for other vertebrate species.
...
PMID:Amphibian oocyte: a model of a possible regulatory mechanism for prostaglandin E2 and prostaglandin F2 alpha synthesis. 754 11
The aim of this study was to clarify the possible involvement of nitric oxide (NO) on prostaglandin (PG) E2-9-ketoreductase activity in the gonadotropin-releasing hormone (GnRH)-dependent PGF2 alpha synthesis by the interrenal gland of the female water frog, Rana esculenta, during the post-reproduction. Interrenal glands were incubated in vitro with GnRH, NO donor (sodium nitroprusside, SNP), and inhibitors of
phospholipase C
(compound 48/80), inositol triphosphate (decavanadate), calmodulin (calmidazolium), NO synthase (L-NAME), and
PGE2-9-ketoreductase
(palmitic acid). Production of PGE2 and PGF2 alpha and NO synthase and
PGE2-9-ketoreductase
activities were determined. GnRH and SNP increased PGF2 alpha production and
PGE2-9-ketoreductase
activity, and decreased production of PGE2 and GnRH increased NO synthase activity. GnRH effects were blocked by all inhibitors, except for palmitic acid, which did not affect NO synthase activity, which is increased by GnRH. This study indicates that NO may be involved in regulation of the R. esculenta post-reproduction through stimulation of
PGE2-9-ketoreductase
activity in GnRH-dependent PGF2 alpha synthesis by the frog interrenal gland.
...
PMID:Role of nitric oxide in gonadotropin-releasing hormone-dependent prostaglandin F2 alpha synthesis by frog (Rana esculenta) interrenal gland during post-reproduction. 965 67
