HELICOBACTER-PYLORI FATTY-ACID CIS 9,10-METHYLENEOCTADECANOIC ACID INCREASES [CA2-KINASE-C AND STIMULATES ACID-SECRETION IN PARIETAL-CELLS(](I), ACTIVATES PROTEIN)

The effect of the Helicobacter pylori (H. pylori) fatty acid cis 9,10- methyleneoctadecanoic acid (MOA) on gastric acid secretion was studied in isolated guinea-pig parietal cells. MOA (1 and 3 mu mol/l) stimula ted basal and enhanced histamine- and dibutyryl cyclic AMP-stimulated acid secretion in parietal cells. MOA increased intracellular free [Ca 2+](i) concentration in a concentration-dependent manner. The source o f [Ca2+](i) was extracellular as demonstrated by depletion of [Ca2+](i ) with EGTA. Furthermore, MOA caused activation of parietal cell prote in kinase C (PKC). The effect of MOA upon PKC activation was [Ca2+](i) -dependent but did not require phosphatidylserine as phospholipid co-f actor. Similarly to the effect of diolein, MOA increased the stimulato ry effect of phosphatidylserine at low [Ca2+](i) concentrations. Treat ment of parietal cells with MOA caused translocation of PKC from the c ytosol to the membrane-associated cell fraction. We propose that MOA s timulates parietal cell acid secretion presumably by an increase of cy tosolic free [Ca2+](i) concentrations and PKC activation.