The new orally active iron chelator ICL670A exhibits a higher antiproliferative effect in human hepatocyte cultures than O-trensox

Eur J Pharmacol. 2006 Jul 17;541(3):129-37. doi: 10.1016/j.ejphar.2006.05.001. Epub 2006 May 11.

Abstract

By comparing the antiproliferative effect of the iron chelators ICL670A and O-trensox in the human hepatoma cell line HUH7 and human hepatocyte cultures, we have shown that ICL670A decreased cell viability, inhibited DNA replication and induced DNA fragmentation more efficiently than O-trensox. O-trensox and ICL670A induced a cell cycle blockade in G0-G1 and S phases respectively. In parallel, ICL670A inhibited polyamine biosynthesis by decreasing ornithine decarboxylase and spermidine/spermine N(1)-acetyltransferase activities. O-trensox increased polyamine biosynthesis and particularly putrescine level by stimulating spermidine-spermine N(1)-acetyltransferase activity which could activate the polyamine retro-conversion pathway. Moreover, the two chelators exhibit some cytotoxic effect in the two culture models; ICL670A was more cytotoxic than O-trensox and higher concentrations of the two chelators were necessary to induce a cytotoxicity in primary cultures versus hepatoma cells. These results suggested that ICL670A has the most efficient antitumoral effect, blocks cell proliferation by a pathway different of O-trensox and may constitute a potential drug for anticancer therapy.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyltransferases / genetics
  • Acetyltransferases / metabolism
  • Apoptosis / drug effects
  • Benzoates / pharmacology*
  • Biogenic Polyamines / metabolism
  • Carcinoma, Hepatocellular / drug therapy
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / pathology
  • Cell Cycle / drug effects
  • Cell Proliferation / drug effects*
  • DNA Replication / drug effects
  • Deferasirox
  • Ethylamines / pharmacology*
  • Hepatocytes / drug effects*
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Hydroxyquinolines / pharmacology*
  • Iron Chelating Agents / pharmacology*
  • Ornithine Decarboxylase / genetics
  • Ornithine Decarboxylase / metabolism
  • RNA, Messenger / metabolism
  • Triazoles / pharmacology*

Substances

  • Benzoates
  • Biogenic Polyamines
  • Ethylamines
  • Hydroxyquinolines
  • Iron Chelating Agents
  • RNA, Messenger
  • Triazoles
  • trensox
  • Acetyltransferases
  • diamine N-acetyltransferase
  • Ornithine Decarboxylase
  • Deferasirox