Figure 2 | Scientific Reports

Figure 2

From: Disruption in glutathione metabolism and altered energy production in the liver and kidney after ischemic acute kidney injury in mice

Figure 2

Liver MPO activity, histology, superoxide, and mitochondrial respiration after AKI. To assess whether AKI included liver inflammation, injury, elevated reactive oxygen species (ROS), or mitochondrial dysfunction, (A) liver MPO activity, (B, C) liver histology, (D) liver superoxide, and (E) mitochondrial respiration were assessed in the liver and were unchanged versus sham in all cases. In contrast, kidney mitochondrial superoxide increased, and kidney mitochondrial respiration was suppressed. Mitochondrial superoxide was assessed with electron paramagnetic resonance (EPR) spectroscopy. Mitochondrial function (O2 flux) was measured by the Oroboros O2K respirometer and the substrates added to the chamber are listed. Significant differences between mitochondrial oxygen consumption were found in the kidney using the substrates succinate, CCCP and rotenone, indicating a defect in complex II during AKI. Data are mean ± SE; statistics by Student’s t-test comparing Sham versus AKI at each time point; n = 6–10 per group, **p < 0.01.

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