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. 2008 Sep 19;283(38):26217–26227. doi: 10.1074/jbc.M803287200

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Copyright © 2008, The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 4. — Young Mclk1⁺^/^- mice have higher mitochondrial oxidative stress and altered TCA cycle. Mitochondria of young Mclk1^+/- mice display high oxidative stress as revealed by accumulation of protein carbonyls (A), higher levels, but not significantly, of lipid peroxidation (B), up-regulation of the major enzymatic antioxidant defenses, such as Se-GPx (C) and manganese-dependent superoxide dismutase (MnSOD; D), and increased ROS production per molecule of reduced O₂ from isolated mitochondria (E). Each bar in the graphs represents the mean ± S.E. of 12 Mclk1^+/+ and 10 Mclk1^+/- animals. The asterisk denotes statistical significance of the difference between Mclk1^+/+ and Mclk1^+/- animals, p < 0.05. F, schematic representation of the effects of Mclk1 heterozygosity on key TCA cycle enzymes. Aconitase (in red) is partially inactivated, and α-ketoglutarate dehydrogenase (α-KGDH, in blue) is up-regulated in Mclk1^+/- animals. Unaffected enzymes are showed in green.