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. Author manuscript; available in PMC: 2017 May 24.
Published in final edited form as: Circulation. 2016 Apr 8;133(21):2038–2049. doi: 10.1161/CIRCULATIONAHA.115.020226

Figure 7.

Figure 7

Disturbed metabolic and redox homeostasis by BCKAs. A, Oxygen consumption in mitochondria isolated from wildtype hearts in absence or presence of 500μM BCKAs. B, Relative oxygen consumption rate in the absence or presence of BCKAs at different concentrations (n=3–8 in each group; *, p<0.05 vs control). C, Superoxide production in isolated cardiac mitochondria (n=4–7 in each group; *, p<0.05, vs control). D and E, Superoxide production in isolated mitochondria (D, n=5–6 in each group) and myocardium (E, n=3 in each group) from wildtype and PP2Cm deficient mice. F, Immunoblotting of total protein oxidation detected by carbonyl groups (left) from tissue lysates of wildtype (WT) and PP2Cm deficient (KO) mouse hearts. G, Principal component analysis (PCA) of metabolomic profiles revealed a distinct genotype-based separation for the heart samples (WT, n=8; KO, n=7). H, List of the top 30 biochemicals that separated different genotypes based on their importance. Error bars represent standard deviation SEM (B C, D, E).