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. Author manuscript; available in PMC: 2007 May 5.
Published in final edited form as: Neuroscience. 2007 Jan 18;145(1):256–264. doi: 10.1016/j.neuroscience.2006.11.065

Figure 5.

Figure 5

Ketones (KB) reduce calcium-induced alterations in mitochondrial bioenergetics, ROS production and NAD+/NADH cycling. (A) Glutamate-mediated influx of calcium into mitochondria was not affected by ketones. Acutely dissociated neurons were incubated with the fluorescent mitochondrial calcium indicator Rhod-2. Exposure to 10 μM glutamate for 10 min (n = 5) increased mitochondrial calcium levels significantly relative to controls (n = 4). The same findings were observed when 1 mM BHB and 1 mM ACA were added (n = 4; ANOVA on ranks with Dunn’s post-hoc analyses; p < 0.05). (B) 0.5 mM calcium significantly increased mitochondrial ROS production and NADH concentrations. The addition of BHB and ACA (1 mM each) reduced both mitochondrial ROS production and NADH levels to baseline. (C) Mitochondrial respiration was assessed using a Clark-type electrode and demonstrated that calcium significantly impaired complex-I (NADH-linked) driven oxygen consumption both in response to the addition of ADP (state III respiration) or carbonyl cyanide p-[trifluoromethoxy]-phenyl-hydrazone [FCCP] (maximum electron transport system capacity; state Va) but did not significantly alter complex-II (FADH-linked) driven maximum electron transport system capacity (state Vb). The inclusion of 1 mM BHB and 1 mM ACA partially reversed this inhibition of respiration. * p < 0.05; ** p < 0.01.