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

Figure 5. Increased oxidative stress and DNA damage in Ppara+/+:HCVcpTg mice at 24 months of age.

Figure 5

(A) Immunohistochemical staining using antibody against 8-OHdG. In Ppara+/+:HCVcpTg mice, some steatotic hepatocytes were positive for 8-OHdG. Original magnification, ×400. (B) Numbers of 8-OHdG–positive hepatocytes. Hepatocyte nuclei stained with anti-8-OHdG antibody were counted in 2,000 hepatocytes of each mouse. Results are expressed as the mean ± SD (n = 6/group). (C) Hepatic content of lipid peroxides. 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. (D) Immunoblot analysis of AOX, CYP4A1, catalase, and Cu, Zn-SOD. The whole-liver lysate used in the experiment in Figure 4E (20 μg protein for AOX and CYP4A1 and 50 μg for others) was loaded in each lane. The band of actin was used as the loading control. Results are representative of 4 independent experiments. A and B indicate full-length and truncated AOX, respectively. The band intensity was quantified densitometrically, normalized by that of actin, and subsequently normalized by that in Ppara+/+ nontransgenic mice. The mean value of the fold changes is expressed under each band. *P < 0.05 compared with Ppara+/+ nontransgenic mice.