Antioxidants stimulate transcriptional activation of the c-fos gene by multiple pathways in human fetal lung fibroblasts (WI-38)

J Cell Physiol. 1998 Sep;176(3):624-33. doi: 10.1002/(SICI)1097-4652(199809)176:3<624::AID-JCP19>3.0.CO;2-Z.

Abstract

We have examined the effects of three structurally distinct antioxidants (N-acetylcysteine [NAC], Trolox C [a water-soluble vitamin E derivative], and nordihydroguaiaretic acid [NGA]) on the expression of the c-fos gene over a 2-hour period. Determination of cellular glutathione concentration (the primary determinant of the cellular redox state) over the same time-course verifies that all the compounds studied cause an increase in cellular reduction potential. The level of c-fos messenger RNA increased rapidly in response to micromolar concentrations of these compounds, reaching a peak in 30-60 minutes. Induction of c-fos expression by these antioxidants is at least partly due to an increase in transcription, as determined by nuclear run-on assay. Down regulation of protein kinase C (PKC) by pretreatment for 24 hours with 500 nm PMA prevents induction by subsequent stimulation with either PMA or NGA. NAC induction of c-fos is unaffected by PMA pretreatment, while Trolox C superinduced c-fos following PMA pretreatment. None of these treatments stimulated translocation of PKC-alpha from the cytosol to the membrane. These results suggest that increasing the intracellular reducing potential induces c-fos expression through multiple pathways.

Publication types

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

MeSH terms

  • Acetylcysteine / pharmacology
  • Antioxidants / pharmacology*
  • Blotting, Northern
  • Carcinogens / pharmacology
  • Chromans / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Fetus / enzymology
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Free Radical Scavengers / pharmacology
  • Gene Expression Regulation / drug effects
  • Glutathione / metabolism
  • Humans
  • Lung / cytology*
  • Masoprocol / pharmacology
  • Naphthalenes / pharmacology
  • Protein Kinase C / metabolism
  • Proto-Oncogene Proteins c-fos / genetics*
  • RNA, Messenger / analysis
  • Signal Transduction / physiology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcriptional Activation / drug effects*

Substances

  • Antioxidants
  • Carcinogens
  • Chromans
  • Enzyme Inhibitors
  • Free Radical Scavengers
  • Naphthalenes
  • Proto-Oncogene Proteins c-fos
  • RNA, Messenger
  • Masoprocol
  • Protein Kinase C
  • Glutathione
  • calphostin C
  • Tetradecanoylphorbol Acetate
  • 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid
  • Acetylcysteine