Suppression of G1 arrest and enhancement of G2 arrest by inhibitors of poly(ADP-ribose) polymerase: possible involvement of poly(ADP-ribosyl)ation in cell cycle arrest following gamma-irradiation

Jpn J Cancer Res. 1994 Nov;85(11):1094-8. doi: 10.1111/j.1349-7006.1994.tb02912.x.

Abstract

Low-dose gamma-irradiation of mouse embryonic fibroblast C3D2F1 3T3-a cells caused G1 arrest along with G2 arrest and inhibition of replicative DNA synthesis. When the cells were cultured in the presence of inhibitors of poly(ADP-ribose) polymerase [EC 2.4.2.30], such as 3-aminobenzamide, benzamide and luminol, G1 arrest of C3D2F1 3T3-a cells was suppressed and enhancement of G2 arrest was observed. In contrast, 3-aminobenzoic acid, a non-inhibitory analog of 3-aminobenzamide, did not suppress G1 arrest following gamma-irradiation. These results suggest that the poly(ADP-ribosyl)ation reaction is critical for the pathway of G1 arrest and is also involved in the pathway of G2 arrest.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzamides / pharmacology
  • Cell Line
  • DNA Damage
  • DNA Repair
  • G1 Phase / drug effects
  • G1 Phase / radiation effects*
  • G2 Phase / drug effects
  • G2 Phase / radiation effects*
  • Gamma Rays
  • Mice
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Poly(ADP-ribose) Polymerases / physiology*

Substances

  • Benzamides
  • Poly(ADP-ribose) Polymerase Inhibitors
  • 3-aminobenzamide
  • Poly(ADP-ribose) Polymerases