Theophylline prevents NAD+ depletion via PARP-1 inhibition in human pulmonary epithelial cells

Biochem Biophys Res Commun. 2005 Dec 30;338(4):1805-10. doi: 10.1016/j.bbrc.2005.10.159. Epub 2005 Nov 2.

Abstract

Oxidative DNA damage, as occurs during exacerbations in chronic obstructive pulmonary disease (COPD), highly activates the nuclear enzyme poly(ADP-ribose)polymerase-1 (PARP-1). This can lead to cellular depletion of its substrate NAD+, resulting in an energy crisis and ultimately in cell death. Inhibition of PARP-1 results in preservation of the intracellular NAD+ pool, and of NAD+-dependent cellular processes. In this study, PARP-1 activation by hydrogen peroxide decreased intracellular NAD+ levels in human pulmonary epithelial cells, which was found to be prevented in a dose-dependent manner by theophylline, a widely used compound in the treatment of COPD. This enzyme inhibition by theophylline was confirmed in an ELISA using purified human PARP-1 and was found to be competitive by nature. These findings provide new mechanistic insights into the therapeutic effect of theophylline in oxidative stress-induced lung pathologies.

MeSH terms

  • Cell Line, Tumor
  • Enzyme Activation
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism*
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Kinetics
  • Lung / cytology
  • Lung / metabolism*
  • NAD / metabolism*
  • Oxidative Stress
  • Poly (ADP-Ribose) Polymerase-1
  • Poly(ADP-ribose) Polymerase Inhibitors*
  • Pulmonary Disease, Chronic Obstructive / drug therapy
  • Theophylline / pharmacology*
  • Theophylline / therapeutic use

Substances

  • Poly(ADP-ribose) Polymerase Inhibitors
  • NAD
  • Hydrogen Peroxide
  • Theophylline
  • PARP1 protein, human
  • Poly (ADP-Ribose) Polymerase-1