Inhibition of neutrophil oxidative metabolism by nimesulide

Agents Actions. 1987 Jun;21(1-2):121-9. doi: 10.1007/BF01974932.

Abstract

Oxygen derived free radical release from activated neutrophils may be in part responsible of tissue damage in the acute phase of inflammation. We have shown that the methane sulfonanilide antiinflammatory agent nimesulide inhibits the respiratory burst of phagocytosing neutrophils without affecting their phagocytic or chemotactic responsiveness. In fact, chemiluminescence and superoxide anion generation by polymorphonuclear leukocytes (PMN) stimulated with zymosan particles or with the synthetic peptide FMLP are inhibited by nimesulide and its 4-OH metabolite in a dose dependent fashion without affecting cell viability. The control of the extracellular flux of radical species by pharmacological compounds may affect the course of inflammation reducing tissue damage. Our data suggest that the inhibition of superoxide anion production by neutrophils is an additional mechanism of action of the antiinflammatory agent nimesulide.

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / metabolism
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Antioxidants / pharmacology
  • Cytochrome c Group / metabolism
  • Depression, Chemical
  • Free Radicals
  • Humans
  • Inflammation
  • Luminescent Measurements
  • N-Formylmethionine Leucyl-Phenylalanine / antagonists & inhibitors
  • Neutrophils / drug effects*
  • Neutrophils / metabolism
  • Oxidation-Reduction
  • Oxygen / metabolism
  • Phagocytosis / drug effects
  • Sulfonamides / metabolism
  • Sulfonamides / pharmacology*
  • Superoxides / biosynthesis
  • Zymosan / antagonists & inhibitors

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antioxidants
  • Cytochrome c Group
  • Free Radicals
  • Sulfonamides
  • Superoxides
  • N-Formylmethionine Leucyl-Phenylalanine
  • Zymosan
  • Oxygen
  • nimesulide