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. Author manuscript; available in PMC: 2011 Aug 15.
Published in final edited form as: Free Radic Biol Med. 2010 Jun 2;49(4):567–579. doi: 10.1016/j.freeradbiomed.2010.04.037

Fig. 8.

Fig. 8

IsoKs affect mitochondrial respiratory parameters. Mitochondrial respiration was measured in the presence of IsoKs (0.5–4 μM). A. Isolated liver mitochondria (0.25 mg/ml) were supplemented with the complex I substrate glutamate/malate (5 mM). The incubation buffer also contained 2 mM KH2PO4, 3 μM EDTA. The rate of mitochondrial respiration in the presence of substrates corresponds only to state 2 (V2). Addition of ADP (200 μM) initiated ATP synthesis coupled to proton reentry across the membrane, which corresponds to state 3 (VADP or V3). ADP exhaustion led to the reduction of respiratory rate and corresponds to state 4 (V4). Addition of DNP (20 μM) is followed by state 4. Data are expressed as a percentage change of respiration parameters in the presence of IsoKs compare with IsoKs untreated mitochondria and plotted as a mean ± sem, N=3, *, p < 0.05. B. RCR was calculated as the ratio between the rates of respiration in state 3 and 4. Data plotted as a mean ± sem, N=3, *, p < 0.05 compare with IsoKs untreated mitochondria.