Abstract
Stimulation of IgE receptors on rat basophilic leukemia cells causes a transient rise and fall of methylated phopholipids, Ca 2+ influx, and release of arachidonic acid previously incorporated into phosphatidylcholine and liberation of histamine. Inhibition of phospholipid methylation by methyltransferase inhibitors, 3-deazaadenosine and homocysteine thiolactone, almost completely blocks the influx of Ca 2+, and release of arachidonic acid and histamine. Stimulation of immunoglobulin E receptors by antigen releases only [ 14C]arachidonic acid but not [ 14C]linoleic acid, [ 14C]oleic acid and [ 14C]stearic acid, all of which were previously incorporated into phospholipids. [ 14C]Arachidonate was found to be incorporated mainly into phosphatidylcholine. The phosphatidycholine rich in arachidonate appeared to be synthesized to a considerable extent by the transmethylation pathway. These findings suggest that in rat basophilic leukemia cells, immunoglobulin E receptors, phospholipid methyltransferases, Ca 2+ ion channel, and phospholipase(s) that cause release of arachidonic acid and the discharge of histamine are associated.
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