Figure 3.

Excessive Reactive Oxygen Species From Mitochondria Mediate Doxorubicin-Induced Endothelial Dysfunction in Conduit Arteries

(A) Mitochondrial reactive oxygen species (ROS) in aortic segments. Representative electron paramagnetic resonance spectra are shown above. (B) Dose-response and (C) peak endothelium-dependent dilation (EDD) to acetylcholine in the presence of the mitochondrial-targeted antioxidant, MitoQ (1.0 μmol/l, 60 min incubation to scavenge mitochondrial-specific reactive oxygen species). (D) Aortic protein abundance of superoxide dismutase-2 (SOD2); representative images from the WES capillary electrophoresis automated Western blot system are shown above. Protein abundance of target proteins are normalized to protein abundance of GAPDH. Data are the mean ± SEM. n = 4 (sham); n = 4 (doxorubicin [DOXO]); n = 5 (DOXO + MitoQ). ∗p < 0.05 vs. sham; ^#p < 0.05 doxorubicin (DOXO) + MitoQ vs. DOXO.