Chlorhexidine was cytotoxic to both neutrophils and red blood cells over a narrow concentration range of 0.01 to 0.02% drug. Serum provided significant protection against the cytotoxic effects of the antimicrobial agent. At a concentration of 0.01%, chlorhexidine acted as a potent activator of the neutrophil's oxidative burst, stimulating the cells to produce oxygen radicals such as superoxide (O2). Chlorhexidine ranging from 10 ' to 10~-caused spontaneous degranulation of neutrophils. If neutrophils were pretreated with chlorhexidine and then activated by the chemoattractant tripeptide FMLP, chlorhexidine inhibited the induced O2 generation and degranulation. If, on the other hand, neutrophils were activated with phorbol myristate acetate (PMA) following chlorhexidine treatment, the antimicrobial agent enhanced both 02~ synthesis and degranulation. It appears that the responsiveness of chlorhexidine-treated neutrophils to subsequent activators is dependent upon the nature of the activator.
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