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However, the mitochondrial content of acetyl-CoA during acetylcarnitine supplementation is the result of acetyl-CoA formation, due to the mass-action of CAT, and utilization of the former

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UGT1A6 is important at low APAP concentrations [16], while UGT1A9 and UGT1A1 contribute the most at toxic doses with UGT1A9 catalyzing within a broad range of pharmacologically relevant APAP concentrations [16,17]