Figure 4. Thioredoxin reductase-2 and mitochondrial ROS supported by a combination of substrates in cardiac and skeletal muscle following HFHS diet and/or exercise.

Rates of mitochondrial H₂O₂ emission (mito-) supported by palmitoyl-l-carnitine + glutamate/malate + succinate in state 3 (i.e. phosphorylating) conditions in the absence and presence of the TxnRd2 inhibitor auranofin are shown for cardiac (A) and red gastrocnemius skeletal muscle (B). Data are shown as means + SEM, n= 5–8 per group. *P < 0.05 vs. Ctl Sed (–auranofin), ‡P < 0.05 vs. HFHS + Ex (–auranofin), **P < 0.05 indicates main effect of auranofin within group and §P < 0.05 vs. Ctl + HFHS Sed (+auranofin).