Fluoride Stimulation of Canine Neutrophils: The Role of Calcium Binding

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Abstract
Neutrophils are known to undergo a burst of metabolic activity in response to particulate and soluble stimuli [during phagocytosis]. Most of these stimuli depend upon Ca in the extracellular medium to exert their maximal effects. A total of 24 mM NaF stimulates the metabolic burst in canine neutrophils as measured by chemiluminescence and CO2 formation from the C-1 position of glucose. Because these phenomena are Ca dependent, the uptake of Ca by neutrophils activated with NaF was determined. Neutrophils suspended in buffer were incubated with 45CaCl2 and exposed to NaF. This caused an increase in cell-associated Ca from 1.89 .+-. 0.43 .times. 10-10 mol/107 cells to 1.06 .+-. 0.15 .times. 10-8 mol/107 cells in 2 min. In comparison, the Ca ionophore A23187 (10-6 M) caused only a modest increase in cell Ca, from 1.89 .+-. 0.43 .times. 10-10 mol/107 cells to 4.89 .+-. 0.85 .times. 10-10 mol/107 cells. When treated with EGTA [ethylene glycol bis-(.beta.-aminoethyl ether)-N,N,N'',N''-tetraacetic acid] (3 mM), NaF-stimulated neutrophils rapidly lost 90% of their cell-associated Ca. Verapamil (3 .times. 10-4 M), a Ca channel blocker, inhibited NaF stimulation of neutrophil metabolism, but did not decrease the magnitude or the rate of the Ca association. The mechanism of NaF stimulation of neutrophil apparently involves massive Ca binding to the external membrane and a subsequent movement of some of this membrane Ca into the cell.

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