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Although with some controversy, the accumulated evidence directly supports an age-related decline in the ability to respond to OS with the activation of the NRF2/ARE signalling pathway, thereby reducing the expression of its target antioxidant genes [327]

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Various genetic polymorphisms in CYP enzymes and their levels of activity may explain why APAP is metabolized with excessive or diminished oxidative capabilities.26,43,44 The enzymes UGT (glucouronidation), SULT, CYP 450, GST, N -deacetylase (deacetylation), NAT2 (deacetylation), and fatty acid amide hydrolase are involved in APAP metabolism and have been shown to be related to both hepatic and nephrotoxic effects of the analgesic medication.45 It appears that genotypic changes of these enzymes leads to potentially different risk/benefit ratios when APAP is ingested

Cell 124 , 471484 (2006)