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. 2017 Dec 14;15:216–227. doi: 10.1016/j.redox.2017.12.006

Fig. 8.

Fig. 8

Partial loss or ablation of GRX2 induces a significant increase in O2•-/H2O2 release from liver and cardiac mitochondria oxidizing succinate. A. Liver (0.3 mg/mL) and cardiac (0.1 mg/mL) mitochondria were diluted in reaction buffer containing succinate (50 µM) and the production of H2O2 was measured using AUR reagent. n = 5, mean±SEM. 1-way ANOVA Fisher's LSD post-hoc test. B. Examination of the high capacity site(s) for O2•-/H2O2 release in liver mitochondria oxidizing succinate. Mitochondria (0.3 mg/mL) were preincubated in KMV (10 mM) or myxothiazol (4 µM) in reaction buffer and then H2O2 production was measured using AUR and pyruvate (50 µM) or 2-oxoglutarate (50 µM) and malate (50 µM). n = 5, mean ± SEM. 1-way ANOVA Fisher's LSD post-hoc test. n = 4, mean ± SEM, 2-way ANOVA Fisher's LSD post-hoc test.