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P-cresol, indoxyl and acetaminophen are substrates for hepatic SULT1A1. Uremic toxins perpetrate interactions with SULT1A1, such that metabolism of substrates can be shunted to alternate metabolic pathways. For example, acetaminophen metabolism may be shunted (dotted line) towards CYP2E1, forming the toxic metabolite NAPQI, and p-cresol metabolism may be shunted (dotted line) towards UGT, forming p-cresol glucuronide.
