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Complementation of mitochondrial electron transport chain by manipulation of the NAD⁺/NADH ratio
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Complementation of mitochondrial electron transport chain by manipulation of the NAD⁺/NADH ratio
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Journal Article
Complementation of mitochondrial electron transport chain by manipulation of the NAD⁺/NADH ratio
2016
Overview
A decline in electron transport chain (ETC) activity is associated with many human diseases. Although diminished mitochondrial adenosine triphosphate production is recognized as a source of pathology, the contribution of the associated reduction in the ratio of the amount of oxidized nicotinamide adenine dinucleotide (NAD⁺) to that of its reduced form (NADH) is less clear. We used a water-forming NADH oxidase from Lactobacillus brevis (LbNOX) as a genetic tool for inducing a compartment-specific increase of the NAD⁺/NADH ratio in human cells. We used LbNOX to demonstrate the dependence of key metabolic fluxes, gluconeogenesis, and signaling on the cytosolic or mitochondrial NAD⁺/NADH ratios. Expression of LbNOX in the cytosol or mitochondria ameliorated proliferative and metabolic defects caused by an impaired ETC. The results underscore the role of reductive stress in mitochondrial pathogenesis and demonstrate the utility of targeted LbNOX for direct, compartment-specific manipulation of redox state.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
/ Electron Transport Chain Complex Proteins - genetics
/ Electron Transport Chain Complex Proteins - metabolism
/ Genetic Complementation Test
/ Humans
/ Lactobacillus brevis - enzymology
/ Lactobacillus brevis - genetics
/ Mitochondrial Diseases - enzymology
/ Mitochondrial Diseases - genetics
/ Multienzyme Complexes - genetics
/ Multienzyme Complexes - metabolism
/ NADH, NADPH Oxidoreductases - genetics
