Poly(ADP-ribose) catabolism in mammalian cells exposed to DNA-damaging agents

Mutat Res. 1989 Sep;218(2):67-74. doi: 10.1016/0921-8777(89)90012-8.

Abstract

DNA damage inflicted by the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, or by UV254nm, stimulated the catabolism of protein-bound poly(ADP-ribose) in the chromatin of cultured hepatocytes. The stimulation was highest at the largest doses of DNA-damaging treatment. As a consequence, the half-life of ADP-ribosyl polymers may drop to less than 41 s. This rapid turnover contrasts with the slow catabolism of a constitutive fraction of polymers exhibiting a half-life of 7.7 h. Our data suggest that post-incisional stimulation of poly(ADP-ribose) biosynthesis in DNA-excision repair is coupled with an adaptation of poly(ADP-ribose) catabolism in mammalian cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzamides / pharmacology*
  • Cells, Cultured
  • Chromatin / drug effects
  • Chromatin / metabolism
  • Chromatin / radiation effects
  • DNA Damage*
  • Kinetics
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Methylnitronitrosoguanidine / pharmacology*
  • Nucleoside Diphosphate Sugars / metabolism*
  • Poly Adenosine Diphosphate Ribose / metabolism*
  • Poly Adenosine Diphosphate Ribose / radiation effects
  • Radiation-Sensitizing Agents / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Ultraviolet Rays*

Substances

  • Benzamides
  • Chromatin
  • Nucleoside Diphosphate Sugars
  • Radiation-Sensitizing Agents
  • Methylnitronitrosoguanidine
  • Poly Adenosine Diphosphate Ribose
  • 3-aminobenzamide