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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
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Th17 Cell Enhances CD8 T-Cell Cytotoxicity via IL-21 Production in Emphysema Mice
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