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. 2022 Apr 7;29(10):1996–2008. doi: 10.1038/s41418-022-00991-4

Fig. 3. Alternative NADH dehydrogenase NDI1 rescues oxygen consumption rate (OCR) inhibition and protects from toxicity of complex I inhibitors.

Fig. 3

A Scheme of NDI1 function when expressed in mammalian cells characterized by defective or inactivated NADH dehydrogenase. B, E, F Representative OCR traces and quantification of basal OCR of Nf1+/+ and Nf1−/− MEFs. The ATP synthase inhibitor oligomycin (0.8 µM), the proton uncoupler carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP, 1 µM) and the respiratory complex I and III inhibitors rotenone (0.5 µM) and antimycin A (1 µM), respectively, were added as indicated. In E, F, AUL12 (4 µM) was added 45 min before recordings. NDI: cells expressing the pWPI-NDI1 construct; EV: cells expressing the pWPI empty vector. C Measurement of complex I activity in control and AUL12-treated mitochondria. D Analysis of mitochondrial ROS levels by MitoSOX staining in control and AUL12-treated (4 mM, 1 h) cells. All experiments in the Figure were carried out on Nf1+/+ and Nf1−/− MEFs. Data are reported as mean ± SD values (n ≥ 3); ***p < 0.001; **p < 0.01 and *p < 0.05 with a Student’s t test analysis or One-way ANOVA followed by Bonferroni post-test (B–D).