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Therefore, it is conceivable that impaired mitochondrial fuel oxidation could occur due to damaged mitochondrial DNA leading to defects in transcription, translation, or activity of enzymes regulating NEFA oxidation and that improving GSH concentrations could protect against such ROS-induced mitochondrial damage

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But stacking two experimental compounds doesn’t solve the underlying issue: Neither has strong human clinical evidence, and neither is expert recommended nor regulated for these uses