Fig. 5

Isolated brain mitochondria exhibit a higher respiratory rate and are differentially affected by ETC. inhibitors compared to liver mitochondria. a Representative trace of brain and liver mitochondrial oxygen consumption using glutamate and malate as a substrate with or without addition of rotenone where indicated. (b–d) Mitochondrial respiration was supported by glutamate and malate (complex I) (b, c) or succinate (complex II) (d, e), respectively. State 2 respiration was monitored before the addition of 0.5 mM ADP to induce state 3 respiration. After achieving maximal state 3 respiration, DPI (10 μM), CMB (10 μM), or rotenone (10 μM) was added. Percent inhibition of respiration achieved by rotenone, DPI, and CMB was calculated for both glutamate and malate (c) and succinate (e) supported respiration by comparing state 3 respiratory rates to stable respiratory rates after inhibitor treatments. For each treatment, n ≥ 3. P values are indicated comparing brain and liver mitochondria for state 2 and state 3 respiratory rates, as well as state 3 respiratory rates after rotenone, DPI, or CMB treatment. Isolated mitochondria (0.4 mg) were used for each experiment. For each treatment, brain mitochondria are compared, where a vs. b vs. c < 0.05; liver mitochondria are compared, where x vs. y vs. z < 0.05