Effect of deferoxamine on DNA synthesis, DNA repair, cell proliferation, and differentiation of HL-60 cells

Leukemia. 1987 May;1(5):437-41.

Abstract

The ribonucleotide reductase inhibitors deferoxamine and hydroxyurea induce monocyte-macrophage cell differentiation in the leukemic cell line HL-60 as judged by the expression of cell surface antigens, nonspecific esterase activity, and morphological changes. Treatment of HL-60 cells with deferoxamine results in inhibition of DNA synthesis and irreversible loss of colony-forming ability. In addition, both deferoxamine and hydroxyurea caused an increase in the number of DNA strand breaks in HL-60 cells. A DNA methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine, also caused cellular differentiation in HL-60 cells associated with DNA strand breaks. These observations are consistent with a role for DNA damage or for inhibition of DNA synthesis and repair in the differentiation process of HL-60 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Surface / analysis
  • Benzamides / pharmacology
  • Cell Cycle / drug effects*
  • Cell Differentiation / drug effects
  • DNA Repair / drug effects*
  • DNA, Neoplasm / biosynthesis*
  • Deferoxamine / pharmacology*
  • Humans
  • Hydroxyurea / pharmacology
  • Leukemia, Myeloid, Acute / pathology
  • Methylnitronitrosoguanidine / pharmacology
  • Neoplasm Proteins / biosynthesis
  • RNA, Neoplasm / biosynthesis
  • Ribonucleotide Reductases / antagonists & inhibitors
  • Tumor Cells, Cultured

Substances

  • Antigens, Surface
  • Benzamides
  • DNA, Neoplasm
  • Neoplasm Proteins
  • RNA, Neoplasm
  • Methylnitronitrosoguanidine
  • 3-aminobenzamide
  • Ribonucleotide Reductases
  • Deferoxamine
  • Hydroxyurea