Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction

Figure 4 ob/ob AMLN hepatocytes display increased numbers of fragmented mitochondria. (A) Transmission electron micrographs (TEM) showing mitochondrial morphology and ultrastructure in the liver. Scale bar = 0.2 μm. Quantification of the number of mitochondria (B) and mitochondrial area (C) from TEM images; (D): Confocal images of HSP60 stained liver sections and quantification of mitochondrial number per cytoplasmic area. Scale bar = 10 μm; (E): Histogram depicting the number of mitochondria per binned mitochondrial length as a percentage of total mitochondria per cell; (F): Mitochondrial content measured by citrate synthase activity in isolated primary hepatocytes; (G): Relative hepatic expression of genes associated with mitophagy; (H): Quantification of mitochondrial genome-encoded CytB or Nd1 relative to nuclear-encoded β-globin from total genomic DNA extracted from the liver. ^aP ≤ 0.05, ^bP ≤ 0.01, vs C57BL6J; ^eP ≤ 0.05, ^fP ≤ 0.01, ^gP ≤ 0.001, ^hP ≤ 0.0001 vs LFD. LFD: Low-fat diet.