Inhibition of mitochondrial function reduces DNA repair in human mononuclear cells

Anat Gafter-Gvili, Michal Herman, Yaacov Ori, Asher Korzets, Avry Chagnac, Boris Zingerman, Benaya Rozen-Zvi, Uzi Gafter*, Tsipora Malachi

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Background: Mitochondria provide ATP and Ca2+ needed for DNA repair, but also produce reactive oxygen species (ROS), which may damage DNA. Aim: To investigate the effect of mitochondrial function inhibition on DNA repair. Method: Five mitochondrial inhibitors acting at various sites of electron transport were studied. Human peripheral blood mononuclear cells, spontaneous and H2O2-indcued DNA repair, as well as %-double-stranded-DNA, were measured. Results: All mitochondrial inhibitors suppressed spontaneous and H2O2-induced DNA repair. However, their effect on %-double-stranded-DNA differed, which is partly related to ROS suppression. Conclusion: Mitochondrial inhibition may enhance efficacy and reduce toxicity of radiation and cytotoxic drugs therapy.

Original languageEnglish
Pages (from-to)219-225
Number of pages7
JournalLeukemia Research
Issue number2
StatePublished - Feb 2011


FundersFunder number
Teva Medical Ltd.


    • %-Double-stranded-DNA
    • 3H-thymidine incorporation
    • DNA breaks
    • HO-indcued DNA repair
    • Human peripheral blood mononuclear cells
    • Mitochondrial inhibitors
    • Spontaneous DNA repair


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