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For instance, Fisher et al.[48] found up to 7-fold differences in the rates of APAP glucoronidation in a sample of 20 human livers, and Court et al.[54] found 15-fold inter-individual variability in APAP glucoronidation rates in liver microsomal fractions

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However, in resistant patients, oxidative stress causes a conformational change in Keap1, leading to the release of NRF2, which translocates to the nucleus and binds to antioxidant response element (ARE), activating the expression of downstream antioxidant genes, including GPX4, NQO1, HO-1 and SOD1 [33], and promoting the synthesis of GSH, as illustrated in Fig

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