Effect of sodium cyanate upon the function of normal human polymorphonuclaer leukocytes.

Sodium cyanate, a drug that prevents sickling of hemoglobin S by virtue of its irreversible carbamylation of the N-terminal amino group of valine, was studied for its effect upon the function of normal human polymorphonuclear luekocytes. In concentrations of 500 and 100 mug/ml, sodium cyanate was found to inhibit killing by neutrophils of Staphylococcus epidermidis and Eschierichia coli but not of Streptococcus faecalis. Viability of cells and phagocytosis were not affected by cyanate; however, production of [14-C] carbon dioxide from [1-14-C] glucose and the iodination of 125-I during phagocytosis were significantly impaired. Cyanate is thought to inbibit the bacterixidal activity of neutrophils by interfering with the oxidative metabolism of gluxose via the hexose monophosphate shunt (theraby decreasing production of H-2-O-2) and by inbibiting iodination of ingested bacteria (either by competing with iodide as the oxidizable cofactor or by inhibiting myeloperoxidase). Since these effects of cyanate were all reversible by washing the nurtrophils free of the drug, it is unlikely that they are due to amino carbamylation.