Doxorubicin causes transient activation of protein poly(ADP-ribosyl)ation in H9c2 cardiomyocytes

Dokl Biochem Biophys. 2015:464:333-7. doi: 10.1134/S1607672915050178. Epub 2015 Oct 31.

Abstract

Possible involvement of the system of protein poly(ADP-ribosyl)ation in the mechanisms of cardiotoxicity of doxorubicin, one of the most frequently used anticancer drug, was studied in cultures of cardiomyocytes H9c2. The treatment of H9c2 cells with doxorubicin (1 µM) led to a transient (after 6 h of incubation) increase in the nuclear level of poly(ADP-ribosyl)ated proteins. The observed data indirectly indicate the development of genotoxic stress in the doxorubicin-treated cells, probably caused by the stimulatory effects of doxorubicin and its metabolites on the production of reactive oxygen and nitrogen species.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibiotics, Antineoplastic / pharmacokinetics
  • Antibiotics, Antineoplastic / toxicity*
  • Cell Line
  • Cell Nucleus / drug effects
  • Cell Nucleus / enzymology
  • Cytoplasm / drug effects
  • Cytoplasm / enzymology
  • Doxorubicin / pharmacokinetics
  • Doxorubicin / toxicity*
  • Enzyme Activators / pharmacokinetics
  • Enzyme Activators / toxicity*
  • Fluorescent Antibody Technique
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / enzymology*
  • Nonlinear Dynamics
  • Poly(ADP-ribose) Polymerases / metabolism*
  • Rats
  • Time Factors

Substances

  • Antibiotics, Antineoplastic
  • Enzyme Activators
  • Doxorubicin
  • Poly(ADP-ribose) Polymerases