Inhibition of mitochondrial function reduces DNA repair in human mononuclear cells |
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Authors: | Anat Gafter-Gvili Michal Herman Yaacov Ori Asher Korzets Avry Chagnac Boris Zingerman Benaya Rozen-Zvi Uzi Gafter Tsipora Malachi |
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Affiliation: | a Department of Nephrology and Hypertension, Rabin Medical Center, Petah Tikva, Israel b Department of Hematology, Rabin Medical Center, Petah Tikva, Israel c Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel |
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Abstract: | BackgroundMitochondria provide ATP and Ca2+ 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 H2O2-indcued DNA repair, as well as %-double-stranded-DNA, were measured.ResultsAll mitochondrial inhibitors suppressed spontaneous and H2O2-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. |
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Keywords: | DNA breaks Spontaneous DNA repair H2O2-indcued DNA repair %-Double-stranded-DNA Mitochondrial inhibitors Human peripheral blood mononuclear cells 3H-thymidine incorporation |
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