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Likewise, in FLAD1-related mitochondrial diseases, although the enzyme that synthesizes FAD is impaired, high-dose riboflavin may saturate the residual activity and promote correct folding, bypassing the synthesis bottleneck

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2.3.3 Enhancement of OS ROS in AKI primarily originate from mitochondrial activity and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complexes (Zorov et al., 2014)