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. 2009 May 8;297(1):H37–H46. doi: 10.1152/ajpheart.00983.2008

Fig. 4.

Fig. 4.

Chronic exposure to Dox. A and B: body weight change in WT (A) and CYP2J2 Tr (B) mice. Animal weights were taken during the chronic Dox protocol; n = 12–15. C: analysis of heart weight-to-body weight ratios (HW:BW) in WT and CYP2J2 Tr mice after chronic Dox treatment (0, 1.5, or 3.0 mg/kg); n = 10–15. *P < 0.05 DOX vs. control of the same genotype; ^P < 0.05 CYP2J2 Tr vs. respective WT. D: semiquantitative PCR analysis of myosin heavy chain (MHC) gene expression. β-MHC:α-MHC expression was quantitated by assessing relative cDNA of both genes from the same individual samples; n = 3. *P < 0.05 Dox vs. control. E: semiquantitative PCR analysis of cardiac ankyrin repeat protein (CARP) gene expression. CARP expression was quantitated by assessing relative cDNA to GAPDH expression from the same individual samples; n = 3. *P < 0.05 Dox vs. control. F: Dox metabolism is increased in CYP2J2 Tr compared with WT hearts and attenuated by the P-450 epoxygenase inhibitor N-methylsulfonyl-6-(propargyloxyphenyl)hexanamide (MS-PPOH, 50 μM). Values are means ± SE; n = 4. *P < 0.05 vs. WT.