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. 2012 Dec 15;17(12):1714–1727. doi: 10.1089/ars.2012.4639

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Copyright 2012, Mary Ann Liebert, Inc.

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FIG. 2. — Role of the mitochondrial energy–redox axis in maintenance of cellular H₂O₂ levels. Reducing equivalents from the tricarboxylic acid cycle flow through the respiratory chain (RC); electron leak accounts for 2%–3% of O₂ consumed in the form of and H₂O₂. Reduction of H₂O₂ is supported by thiol-based systems, for which the ultimate reductant is NADPH. Sources of mitochondrial NADPH: nicotinamide nucleotide transhydrogenase (NNT), isocitrate dehydrogenase-2 (IDH₂), and malic enzyme. Domain-specific signaling entailing regulation of redox-sensitive JNK- and insulin/IGF1 signaling (IIS) pathways,

Inline graphic — Role of the mitochondrial energy–redox axis in maintenance of cellular H₂O₂ levels. Reducing equivalents from the tricarboxylic acid cycle flow through the respiratory chain (RC); electron leak accounts for 2%–3% of O₂ consumed in the form of and H₂O₂. Reduction of H₂O₂ is supported by thiol-based systems, for which the ultimate reductant is NADPH. Sources of mitochondrial NADPH: nicotinamide nucleotide transhydrogenase (NNT), isocitrate dehydrogenase-2 (IDH₂), and malic enzyme. Domain-specific signaling entailing regulation of redox-sensitive JNK- and insulin/IGF1 signaling (IIS) pathways,