• Leukemia research · Feb 2011

    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, and Tsipora Malachi.
    • Department of Hematology, Rabin Medical Center, Petah Tikva, Israel.
    • Leuk. Res. 2011 Feb 1; 35 (2): 219-25.

    BackgroundMitochondria provide ATP and Ca(2+) needed for DNA repair, but also produce reactive oxygen species (ROS), which may damage DNA.AimTo investigate the effect of mitochondrial function inhibition on DNA repair.MethodFive mitochondrial inhibitors acting at various sites of electron transport were studied. Human peripheral blood mononuclear cells, spontaneous and H(2)O(2)-induced DNA repair, as well as %-double-stranded-DNA, were measured.ResultsAll mitochondrial inhibitors suppressed spontaneous and H(2)O(2)-induced DNA repair. However, their effect on %-double-stranded-DNA differed, which is partly related to ROS suppression.ConclusionMitochondrial inhibition may enhance efficacy and reduce toxicity of radiation and cytotoxic drugs therapy.Copyright © 2010 Elsevier Ltd. All rights reserved.

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