Cardiac MAO-A inhibition reduces catecholamine levels and oxidation of PKA, CaMKII and overall oxidative stress in the stress heart. (A) Total catecholamine concentration in the WT and cMAO^def heart tissue after epinephrine/caffeine challenge are shown (N = 6–7 mice for each genotype). Representative immunoblots (B) and quantification of oxidized (C) and non-oxidized (D) PKA-RII and PKA-C after epinephrine/caffeine challenge are shown (N = 6–7 mice for each genotype). Immunoblots (E) and densitometric quantification (F) of ox-CaMKII and total CaMKII after epinephrine/caffeine challenge are shown (N = 4 mice for each genotype). Oxidized CaMKII is normalized to total CaMKII protein. (G) OxyBlot analysis of total protein oxidation (left) as a marker of oxidative stress in heart lysates after epinephrine/caffeine challenge. Stain-free gel (right) was used for total protein loading control. (N = 4 mice for each genotype). (H) Lane intensities in OxyBlot were normalized to the corresponding loading controls and ratios were used to indicate total protein carbonyl levels. Data are represented as mean ± SEM. Data are analysed by unpaired t-test. P-values of comparisons are shown in the graph.