Degradation of hyaluronic acid by neutrophil derived oxygen radicals is stimulus dependent.

A disparity has been noted between the flux of superoxide generated by neutrophils and the effects of those radicals on a typical macromolecular substrate, hyaluronic acid (HA). To further investigate this phenomenon, comparative degradation studies were conducted using phorbol myristate acetate (PMA), which caused neutrophils to readily degrade HA, and digitonin, a stimulus which, like PMA, produced a sustained superoxide flux but which did not affect HA. The differential effects of the 2 stimuli could be related to concomitant release of peroxidase activity. The implications of this mechanism for in vivo oxygen radical effects are discussed.