FIG. 4.

TxnRd2, mitochondrial ROS generation, and PUFA-derived carbonyl stress in atrial myocardium. Shown in (A) are representative immunoblots of TxnRd2 in atrial tissue homogenate from 6 individual Ctl and n-3 PUFA-treated patients, with Tubulin as the loading control. In (B) is densitometry analysis of TxnRd2 in whole atrial tissue from both groups (N=8–10). In (C) are rates of mitochondrial ROS generation (JH₂O₂) coming from the ETS in permeabilized myofibers supported by PM+100 μM ADP, in the absence and presence of TxnRd2 inhibitor auranofin. In (D) is the rate of MAO activity (with tyramine-supported H₂O₂ production as index) in atrial tissue homogenate from both treatment groups. Protein carbonyl adducts in atrial tissue formed by (E), n-6 PUFA-derived aldehyde 4-hydroxynonenal (HNE), and (F), n-3 PUFA-derived aldehyde 4-hydroxyhexenal (HHE), are shown for both treatment groups. Raw data are shown for enzyme activity and PUFA-derived carbonyl adducts in both treatment groups, along with the mean (faint horizontal line). N=8–12 for each group, for all experiments. *p<0.05 versus Ctl, **p<0.01 versus Ctl, #p<0.05 versus. no Auranofin.