AI Article Synopsis
- The decline in electron transport chain (ETC) activity is linked to various human diseases, primarily due to reduced ATP production and uncertain impacts on NAD(+)/NADH ratios.
- Researchers employed a NADH oxidase from Lactobacillus brevis (LbNOX) to selectively boost the NAD(+)/NADH ratio in human cells, affecting key metabolic processes and signaling.
- By expressing LbNOX in either the cytoplasm or mitochondria, they were able to improve growth and metabolism in cells with ETC impairments, highlighting the importance of redox balance in mitochondrial health.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850741 | PMC |
| http://dx.doi.org/10.1126/science.aad4017 | DOI Listing |
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