Figure 3

Oxidative stress leads to the accumulation of 2-AB in hearts, reflecting GSH homeostasis.

(a–c) H₂O₂ increased intracellular levels of 2-AB (a) and GSH (c) in the cells as well as 2-AB levels in the medium (b). Cells were treated with 0.1 mM H₂O₂ for 24 h and the levels of 2-AB and GSH were measured. Bars represent the mean ± s.d. (n = 3). (d) %FS as assessed by echocardiography at 5 days is presented. e, f, Increased 2-AB levels in plasma (e) and hearts (f) in DOX-injected mice. Bars indicate the mean ± s.d. (n = 4, control; n = 6, DOX-injected mice in (e); n = 3, control; n = 7, DOX-injected mice in (f)). (g) Correlation between 2-AB concentration in plasma and %FS. (h) ROS production in control and DOX-injected heart homogenates detected by lucigenin-enhanced chemiluminescence in the presence or absence of SOD, a ROS scavenger. (i) Glutathione levels in heart tissues of DOX-injected mice (n = 4, control; n = 5 DOX-injected mice). %FS, percentage of fractional shortening; DOX, doxorubicin; ROS, reactive oxygen species; SOD, superoxide dismutase. *P < 0.05, **P < 0.01, ***P < 0.0001. n.s., not significant. P-values were determined by unpaired two-tailed Student’s t-tests.