The uptake of a substituted acridone by rat mast cells in relationship to histamine release: a possible indicator of exocytosis-induced expansion of the plasma membrane.

A substituted acridone, 10-(2-dimethylaminopropyl)-9-acridone HCl (M-129), was taken up by isolated rat peritoneal and pleural mast cells in direct relationship to the degree of selective histamine release induced by compound 48/80. Other selective releasing agents, i.e., polymyxin B and anti-rat mast cell serum, also augmented uptake of M-129. Augmented uptake of M-129 was inhibited by measures that inhibited selective histamine release, i.e., cold, brief heating of the mast cells, N-ethylmaleimide and ninhydrin. 48/80 did not agument uptake of M-129 in rat erythrocytes or in rat serous fluid cells from which mast cells had been removed. M-129 taken up by mast cells was readily removed by two to three washes. Augmented uptake induced by 48/80 was specific for M-129 and acridone itself. Related compounds, i.e., a quaternary acridone derivative [10-(2-triethylaminoethyl)-9-acridone iodide] (M-231), acridine and acridan did not show augmented uptake. There was no relationship between heptane-water partition coefficients and uptake. It is postulated, based on estimates of cell membrane area, that M-129 is loosely bound to plasma membrane and that the augmented uptake associated with selective histamine release from rat mast cells is due to expanded plasma membrane that results from irreversible or slowly reversible exocytosis.