Oxidative Stress Contributes to Endothelial Dysfunction in Mouse Models of Hereditary Hemorrhagic Telangiectasia

Figure 4

Mitochondrial and NADPH-dependent ROS production does not differ between mutant and wild-type mice. Results are expressed as a percentage of the respective control values in the absence of inhibitor. (a) and (b) Antimycin, 50 μM, inhibited mitochondrial ROS production to the same level in tissues of both Eng ^+/−, Alk1 ^+/− and respective wild-type mice. 𝑁=5–11/group for Eng mice and 5–15/group for Alk1 mice, except for liver samples from Alk1 ^+/+ mice, where 𝑁=4. (c) and (d) Apocynin, 100 μM, inhibited NADPH-oxidase dependent H₂O₂ production in tissues of both mutant and wild-type mice. 𝑁=5–8/group for both Eng and Alk1 mice, except for heart samples from both groups of mice, where 𝑁=4. *𝑃<0.05, **𝑃<0.01, ***𝑃<0.001, and ^†𝑃<0.1 versus corresponding control values (samples without inhibitor).

(a)

(b)

(c)

(d)