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. 2013 Dec 26;289(6):3339–3351. doi: 10.1074/jbc.M113.538157

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FIGURE 6. — Oxidative DNA damage kills VHL-defective renal cancer cells by exhausting the cellular pool of ATP. A, reduced NAD⁺ levels at different time points after treating VHL-defective RCC10 cells overexpressing VHL or the empty vector with Vc. Vc was added for 1 h (also in B–E). The mean ± S.D. of four independent experiments is shown (also in C–E). Ctrl, control; P, time post-treatment with Vc. B, the PARP inhibitors 3-aminobenzamide and nicotinamide (added 2 h before Vc) reduce Vc-induced toxicity in VHL-defective RCC10 cells. Cell survival (percent) was measured by counting viable cells and is represented as relative to untreated cells (also in D and E). The mean ± S.D. of three independent experiments is shown. C, reduced ATP levels at different time points after treating VHL-defective RCC10 cells overexpressing VHL or the empty vector with Vc. D, DCA (added 48 h before Vc) reduces Vc-induced toxicity in VHL-defective RCC10 cells. E, oligomycin (added 3 h before Vc) increases Vc-induced toxicity in VHL-defective RCC10 cells overexpressing VHL. *, p < 0.05; **, p < 0.01; ***, p < 0.001.