Induction of nuclear factor kappa B after low-dose ionizing radiation involves a reactive oxygen intermediate signaling pathway

Radiat Res. 1994 Oct;140(1):97-104.


Reactive oxygen intermediates (ROIs) have been found to be the messengers in the activation of the kappa B transcription regulator in mitogen- or cytokine-stimulated cells, operating in conjunction with or independently of various other mechanisms; these include Ca(++)-dependent and PKC-dependent cytoplasmic signaling pathways. We have recently reported that low-dose ionizing radiation induces NF-kappa B in human lymphoblastoid 244B cells. Since ionizing radiation generates free radicals in cells, we have investigated whether the ROIs generated by ionizing radiation induce NF-kappa B activity, and also whether they do so by a similar mechanism as in cells treated with PMA or H2O2. The results not only confirm a previous observation from our laboratory that low-dose ionizing radiation (0.1-2.0 Gy) activates kappa B transcription factor transiently with a maximal induction at 0.5 Gy exposure, but also demonstrate mechanistically that the activation of NF-kappa B by low-dose ionizing radiation can be inhibited considerably by the antioxidant N-acetyl-L-cysteine, indicating that at least the major part of the activation process is mediated by ROIs. These findings support the idea that ROIs can regulate the kappa B elements which in turn can serve as response elements for oxidant stress.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acetylcysteine / pharmacology
  • Base Sequence
  • Cell Survival / radiation effects
  • Cells, Cultured
  • DNA / metabolism
  • DNA Damage
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Molecular Sequence Data
  • NF-kappa B / metabolism*
  • NF-kappa B / radiation effects
  • Reactive Oxygen Species / metabolism*
  • Tetradecanoylphorbol Acetate / pharmacology


  • NF-kappa B
  • Reactive Oxygen Species
  • DNA
  • Hydrogen Peroxide
  • Tetradecanoylphorbol Acetate
  • Acetylcysteine