Spontaneous DNA repair in human mononuclear cells is calcium-dependent

Yaacov Ori, Michal Herman, Avry Chagnac, Tsipora Malachi, Uzi Gafter, Asher Korzets

Research output: Contribution to journalArticlepeer-review


Spontaneous DNA repair in peripheral blood mononuclear cells (PBMC) has been recently described. The aim of this study was to evaluate whether spontaneous DNA repair is Ca2+-dependent, as in vitro-stimulated DNA repair. Spontaneous DNA repair in PBMC was measured in a 1 mM Ca2+ medium. The effect of extracellular Ca2+ chelation by EGTA, intracellular Ca2+ chelation by bapta-AM, and Ca2+ loading by the ionophore A23187 was examined. The signal transduction pathway was evaluated by inhibiting protein tyrosine kinase with genistein, calmodulin with W7, and calcineurin with cyclosporin A and tacrolimus. Extracellular Ca 2+ chelation had no effect on spontaneous DNA repair, while both intracellular chelation and calcium overloading inhibited the DNA repair. Inhibition of protein tyrosine kinase, calmodulin or calcineurin reduced DNA repair. In conclusion, spontaneous DNA repair is mainly Ca2+- dependent at a narrow range of intracellular Ca2+ concentrations. The signal transduction cascade includes protein tyrosine kinase, calmodulin, and calcineurin.

Original languageEnglish
Pages (from-to)842-846
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - 28 Oct 2005


  • Ca chelation
  • Ca loading
  • Calcineurin
  • Calcium
  • Calmodulin
  • DNA repair
  • Tyrosine kinase


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