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. 2015 May 7;5:216–224. doi: 10.1016/j.redox.2015.05.001

Fig. 2.

Fig. 2

The effect of auranofin on the apparent kinetics of H2O2 metabolism by rat skeletal muscle mitochondria. (A) Auranofin (2 µM) increases VappP across several substrate conditions. Data are mean±SEM (n=4–5), significant increase due to auranofin (p<0.05). (B) The auranofin dependent increase in H2O2 efflux is strongly proportional to the apparent rate of H2O2 efflux in control mitochondria, consistent with a [H2O2]matrix dependent consumer. Data mean±SEM (n=4–5) with auranofin-induced increase calculated as the difference in H2O2 efflux between the same mitochondria in the presence or absence of 2 µM auranofin to inhibit thioredoxin dependent peroxidase capacity. (C) The rate of extramitochondrial H2O2 disappearance (V Cmaxapp) is substrate dependent and inhibited by auranofin (2 µM) in all cases. Data are mean±SEM (n=3–5), significant decrease due to auranofin (p <0.05). BLD=below limit of detection (i.e. not different from zero). (D) Comparison between VappP and VappCmax in muscle mitochondria respiring on different substrates. Control (black) or auranofin (grey) values are taken from Fig. 2A and C with each substrate condition indicated by a different symbol. Linear regressions are shown to illustrate the relationship between apparent rates of production and consumption.