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. 2008 Feb 1;118(2):683–694. doi: 10.1172/JCI33594

Figure 3. Analyses of mitochondrial abnormalities.

Figure 3

(A) Lignoceric and palmitic acid β-oxidation activities in 9-month-old mice. Results are expressed as the mean ± SD (n = 6/group). *P < 0.05 compared with Ppara+/+ nontransgenic mice; **P < 0.05 compared with Ppara+/–:HCVcpTg mice; #P < 0.05 compared with Ppara–/–:HCVcpTg mice. (B) Electron microscopic features of hepatic mitochondria of 9-month-old HCVcpTg mice. Upper and lower rows show a lower and higher magnification, respectively. In Ppara+/+:HCVcpTg mice, some mitochondria showing discontinuance of outer membranes (arrows) and amorphous inner structures were observed. In Ppara+/–:HCVcpTg and Ppara–/–:HCVcpTg mice, mitochondria appeared normal; the scale bars represent 200 nm (top) and 30 nm (bottom), respectively. (C) Immunoblot analysis of cytochrome c in 9-month-old mice. Whole-liver lysate, mitochondrial fraction, or cytosolic fraction (50 μg protein) was loaded in each well. Results are representative of 4 independent experiments. (D) Immunoblot analysis of representative mitochondrial β-oxidation enzymes using a mitochondrial fraction prepared from 9-month-old mouse livers. The mitochondrial fraction (20 μg protein) was loaded in each well. Results are representative of 4 independent experiments. The band intensity was quantified densitometrically and normalized by that in Ppara+/+ nontransgenic mouse. The mean value of the fold changes is shown under the representative band. LACS, long-chain acyl-CoA synthase; CPT, carnitine palmitoyl-CoA transferase.