Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-alpha

Biochem J. 1989 Oct 15;263(2):539-45. doi: 10.1042/bj2630539.


Human fibroblasts in primary culture released reactive oxygen species upon stimulation with cytokines such as interleukin-1 alpha (IL-1) or tumour necrosis factor-alpha (TNF). The primary radical produced was O2.- as determined by e.s.r. spin trapping and cytochrome c reduction. In contrast to the oxidative burst in granulocytes and monocytes, radical formation took place continuously for at least 4 h. Low-level chemiluminescence was increased by stimulation with IL-1 and TNF. Spectral characteristics and tests with azide led to the conclusion that the photoemissive species were excited carbonyls and not singlet oxygen. Further, there was a liberation of ethane from the cells. Radical production and light emission were not altered by either xanthine or allopurinol, nor by azide, cyanide or rotenone. O2.- production increased in the presence of NADH or NADPH, making an NAD(P)H oxidase a likely source.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytochrome c Group / metabolism
  • Electron Spin Resonance Spectroscopy
  • Ethane / metabolism
  • Fibroblasts / metabolism*
  • Free Radicals
  • Humans
  • Hydrogen Peroxide / metabolism
  • Interleukin-1 / pharmacology*
  • Kinetics
  • Luminescent Measurements
  • NAD / pharmacology
  • NADP / pharmacology
  • Oxidation-Reduction
  • Oxygen / metabolism*
  • Superoxides / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*


  • Cytochrome c Group
  • Free Radicals
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • NAD
  • Superoxides
  • NADP
  • Hydrogen Peroxide
  • Ethane
  • Oxygen