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.
Weitz
Z
Z
Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 11042.
Moak
S A
SA
Greenwald
R A
RA
D004072:Digitonin / Q000494:pharmacology; D005609:Free Radicals; D006801:Humans; D006820:Hyaluronic Acid / Q000378:metabolism*; D009504:Neutrophils / Q000201:enzymology / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D013268:Stimulation, Chemical; D013481:Superoxides / Q000096:biosynthesis; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014783:Viscosity
D005609:Free Radicals; D013481:Superoxides; D006820:Hyaluronic Acid; D009195:Peroxidase; D004072:Digitonin; D013755:Tetradecanoylphorbol Acetate; D010100:Oxygen