Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) are the maj
or phospholipids of the gastric mucosal surface barrier and chiefly or
iginate from mucous cells. Among these phospholipids PC with palmitic
acid as its hydrophobic moieties is believed to protect the gastric mu
cosa by its hydrophobic properties. We investigated the phospholipid s
ynthesis of isolated porcine gastric mucous cells in vitro and incubat
ed them in the presence of radiolabelled precursors. Incorporation of
H-3-choline into PC and of C-14-ethanolamine into PE was linear at 1,
10, and 100 mu mol/l substrate concentration for at least 6 h. Half-ma
ximal rate of precursor incorporation was achieved at 21 and 15 mu mol
/l of choline and ethanolamine, respectively. Ethanolamine inhibited P
C synthesis and choline inhibited PE synthesis. A small amount of radi
oactivity originating from C-14-ethanolamine and from the methyl group
s of H-3-methionine were incorporated into PC. Palmitic acid was incor
porated into PC more than PE. Indometacin did not influence the de nov
o synthesis of PC and PE via the Kennedy pathway, but inhibited the in
corporation of H-3-methionine into PC. These results indicate that in
gastric mucous cells PC and PE synthesis de novo depends on the concen
trations of choline and ethanolamine. The palmitic acid content of PC
depends on the availability of palmitic acid as a substrate: indometac
in-induced mucosal damage is not explained by modulation of phospholip
id synthesis de novo.