AMPHIBIAN OOCYTE - A MODEL OF A POSSIBLE REGULATORY MECHANISM FOR PROSTAGLANDIN E(2) AND PROSTAGLANDIN-F2-ALPHA SYNTHESIS

Citation
A. Gobbetti et M. Zerani, AMPHIBIAN OOCYTE - A MODEL OF A POSSIBLE REGULATORY MECHANISM FOR PROSTAGLANDIN E(2) AND PROSTAGLANDIN-F2-ALPHA SYNTHESIS, Journal of Endocrinology, 145(2), 1995, pp. 235-241
Citations number
37
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
145
Issue
2
Year of publication
1995
Pages
235 - 241
Database
ISI
SICI code
0022-0795(1995)145:2<235:AO-AMO>2.0.ZU;2-P
Abstract
To clarify the possible mechanisms regulating prostaglandin E(2) (PGE( 2)) and prostaglandin F-2 alpha (PGF(2 alpha) synthesis, the effects o f gonadotropin-releasing hormone (GnRH) and substance P (SP) on the re lease of these two prostaglandins were studied in the oocytes of the c rested newt, Triturus carnifex. Full-grown oocytes of T. carnifex, hee d from follicular cells, were incubated in the presence of GnRH or SP and of the inhibitors of several enzymes involved in the release of ar achidonic acid (AA) and in the conversion of AA into PGE(2) and PGF(2 alpha). In parallel, the same experiments were performed on oocytes wi th membrane phospholipids labelled with [H-3]AA. In addition, the PGE( 2)-9-ketoreductase activity was evaluated through the conversion of [H -3]PGE(2) into [H-3]PGF(2 alpha). The results showed that GnRH and SP could regulate prostaglandin synthesis through the activation of phosp holipase C and diacylglycerol lipase, and through the modulation of PG E(2)-9-ketoreductase in the oocytes of T. carnifex. In particular, GnR H enhances the activity of PGE(2)-9-ketoreductase with a consequent in crease in PGF(2 alpha), while SP inhibits the enzyme which leads to an increase in PGE(2). A similar mechanism could also be hypothesized fo r other vertebrate species.