Fig. 5 | Nature Communications

Fig. 5

From: The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury

Fig. 5

Loss of MCJ prevents APAP-induced inhibition of respiratory supercomplexes and ROS generation in liver. a Complex I OCR in WT and MCJ KO liver mitochondria at basal conditions (n = 3). b Complex I OCR in WT and MCJ KO liver mitochondria after APAP treatment (n = 3). c Mitochondrial ROS in WT and MCJ KO hepatocytes treated with APAP (6 h) and Rotenone (complex I inhibitor) (3 h) using MitoSOX dye. BN-PAGE of digitonin-solubilized mitochondrial extracts from WT and MCJ KO hepatocytes d, e livers treated with APAP transferred into a membrane and immunoblotted for NDUFA9 protein. Immunoreactivity within the supercomplex (SC) region and the monomeric complex I (CI) is shown. f Cell death was evaluated using TUNEL in WT and MCJ KO hepatocytes treated with APAP (9 h) and Rotenone (3 h). Values are represented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (Student’s t test) (MCJ KO vs. WT and APAP + Rotenone vs. APAP). Triplicates were used for experimental condition