Skip to main content
. 2021 Sep 8;12(9):839. doi: 10.1038/s41419-021-04128-2

Fig. 5. CISD3 depletion presents a metabolic reprogramming toward glutaminolysis.

Fig. 5

A Cell viability detection in control and CISD3-silenced cells at the presence or absence of indicated chemicals (7.5 µM Erastin, 10 µM C968, and 1 mM GPNA). B Fuel dependency assay for glucose and glutamine in control and CISD3-silenced cells. C After the glutamine oxidation pathway was inhibited by C968, the oxygen consumption (OCR) of basal and max respiration was monitored by Agilent Seahorse XFe24 Analyzer. The inhibition rate of OCR by C968 in control and CISD3-silenced cells was calculated. D, E Cell viability and cellular lipid peroxides detection in the control and CISD3-silenced cells at the presence or absence of indicated chemicals; (7.5 µM Erastin, 10 µM Rotenone (Rot), 2 mM DBM, 2.5 µM Antimycin A (Anti A), 15 mM NaN3, 5 µM CCCP). (F-I) Cell viability, lipid peroxides, cellular ROS, and mitochondrial ROS in control and CISD3-silenced cells were measured under the treatment of 7.5 µM erastin, at the presence or absence of 0.5 µM MitoQ or 0.2 µM SKQ1. The values are presented as means ± SD from three independent experiments. *P < 0.05, **P < 0.01 versus control or between different groups.