Enkephalin degradation by enkephalinergic neuroblastoma cells. Involvement of angiotensin-converting-enzyme.
Degradation of tritiated [Leu5]enkephalin was studied in cultures of neuroblastoma cells (clone N1E-115). Incubation of cells in suspension revealed Tyr as the main tritiated metabolite; however, Tyr-Gly-Gly and Tyr-Gly were detectable as well. In a crude membrane preparation of the neuroblastoma cells the level of Tyr is reduced to 13% and that of Tyr-Gly to 10% of the initial value, whereas Tyr-Gly-Gly is increased to about 5 times the initial value. Of the degraded enkephalin, 66% was accounted for by the formation of Tyr, 30% by the formation of Tyr-Gly-Gly and 4% by the formation of Tyr-Gly. The production of Tyr was inhibited by bestatin, an inhibitor of aminopeptidases, and that of Tyr-Gly-Gly by captopril, an inhibitor of angiotensin-converting-enzyme. The results prove the ability of neuroblastoma cells (N1E-115) to degrade enkephalin by aminopeptidase and the membrane-bound angiotensin-converting-enzyme.
D000626:Aminopeptidases / Q000037:antagonists & inhibitors / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D004743:Enkephalin, Leucine / Q000378:metabolism*; D006868:Hydrolysis; D007930:Leucine / Q000031:analogs & derivatives / Q000494:pharmacology; D051379:Mice; D009447:Neuroblastoma / Q000378:metabolism* / Q000648:ultrastructure; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D015244:Thiorphan; D008625:Tiopronin / Q000031:analogs & derivatives / Q000494:pharmacology
D000806:Angiotensin-Converting Enzyme Inhibitors; D004743:Enkephalin, Leucine; D002216:Captopril; D015244:Thiorphan; D008625:Tiopronin; D000626:Aminopeptidases; D007703:Peptidyl-Dipeptidase A; D007930:Leucine; C012211:ubenimex