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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: DNA Repair (Amst). 2019 Aug 7;82:102675. doi: 10.1016/j.dnarep.2019.102675

Fig. 4. Inhibition of APE1-endonuclease activity impairs mitochondrial activity in a p53-dependent manner.

Fig. 4.

(A and B) HCT-116 p53+/+ and p53−/− cells were seeded in a Seahorse XF-24 analyzer and treated with 0.5 μM of Compund#3 for 48 h. Untreated cells were treated with DMSO. (A) Real-time oxygen consumption rate (OCR) was determined during sequential treatments with oligomycin (ATP-synthase inhibitor), FCCP (uncoupler of oxidative phosphorylation), rotenone (complex I inhibitor) and antimycin-A (complex III inhibitor). (B) The rates of basal respiration, ATP-coupled respiration, spare respiratory capacity and maximal respiration were quantified by normalization of OCR level to total protein content. Data represent means±SEM (n=3). Data were evaluated statistically by two-tails Student t-test. Resulting p-value is indicated (* p<0.05, *** p<0.005).