Some new prospects in the mechanism of control of arachidonate metabolism in human placenta and amnion

• Published in: Prostaglandins Vol. 22; no. 6; pp. 979 - 1002
• Main Authors: Dembélé-Duchesne, M.J., Thaler-Dao, H., Chavis, C., Crastes de Paulet, A.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.1981
• Subjects: Amnion - metabolism; Arachidonic Acid; Arachidonic Acids - metabolism; Dinoprostone; Female; Gas Chromatography-Mass Spectrometry; Humans; Imidazoles - pharmacology; Intramolecular Oxidoreductases; Isomerases - metabolism; Placenta - metabolism; Platelet Aggregation; Pregnancy; Prostaglandin Endoperoxides - metabolism; Prostaglandin Endoperoxides, Synthetic - metabolism; Prostaglandin H2; Prostaglandin-E Synthases; Prostaglandins E - metabolism; Prostaglandins H - metabolism; Thromboxane B2 - metabolism; Thromboxane-A Synthase - metabolism; PPP; p-CMB; BSV; OH-FA; BSTFA; ADP; MNNG; PRP
• ISSN: 0090-6980
• DOI: 10.1016/0090-6980(81)90026-5

The conversion of (1- 14C) PGH 2 was studied in human placental and fetal membrane cellular preparations (tissue fragments, homogenate, cytosol, microsomes). Placental and amnion homogenates convert labelled PGH 2 into PGE 2 through a very active PGE 2 isomerase. However isolated placental microsomes do not metabolise PGH 2 into PGE 2 but into T×A 2 (identified as T×B 2 by GC-MS) and presumably 12-HHT. This microsomal T×A 2 synthetase is not active in the whole tissue nor in the homogenate. Placental cytosol gives mainly PGD 2. No conversion into PGI 2 (identofied as 6 keto PGF 1α) nor PGF 2α was observed in any fraction. Some aspects of PG synthesis regulation by the placental cytosol were studied: the cytosol contains a heat-stable factor that inhibits T×A 2 synthesis and shifts PGH 2 placental microsome metabolism towards PGE 2. In addition the placental cytosol inhibits human platelet-aggregation through a heat-labile factor which is not PGI 2 nor PGD 2. A multiple step regulation of the various PG metabolites synthetised from arachidonic acid in the placenta can be outlined and its physiological implications are discussed.