Research Paper Volume 2, Issue 11 pp 843—853

Activation of mitochondrial energy metabolism protects against cardiac failure

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Figure 1. Over-expression of frataxin induces mito-chondrial metabolism and ROS defense in the heart. (A) Representative anti-hemagglutinin immunoblot showing several tissues from a transgene-negative littermate (“-”) and a transgenic (“+”) animal each. “Control” is a previously published cell line over-expressing frataxin [20]. (B) Aconitase activity measured in murine heart samples. Grey bars indicate wild-type (WT) and white bars indicate frataxin-transgenic (FX) animals (also applies to subsequent figures). (C) ATP, (D) NADH, (E)) NADPH, (F) reduced glutathione (GSH) and (G) thiobarbituric acid reactive substances (TBARS) contents in the hearts of wild-type and frataxin-transgenic animals. Error bars represent S.E.M., *p < 0.05, **p < 0.01, ***p < 0.001 (applies to this and all subsequent figures) (n=4).