Allyn Bryan

Abstract Acetaminophen (AAP) is metabolized by a variety of pathways such as sulfation, glucuronidation, and fatty acid amide hydrolase–mediated conversion to the active analgesic metabolite AM404. CYP2E1-mediated metabolism to the hepatotoxic reactive metabolite NAPQI (N-acetyl-p-benzoquinone imine) is a minor metabolic pathway that has not been linked to AAP therapeutic benefits yet clearly leads to AAP liver toxicity.

Abstract Acetaminophen (AAP) is metabolized by a variety of pathways such as sulfation, glucuronidation and fatty acid amide hydrolase-mediated conversion to the active analgesic metabolite AM404. CYP2E1-mediated metabolism to the hepatotoxic reactive metabolite NAPQI (N-acetyl-p-benzoquinone imine) is a minor metabolic pathway that has not been clearly linked to AAP therapeutic benefits yet definitely leads to AAP liver toxicity.

2. Methods Bone marrow macrophage differentiation. C57bl/6 mice were sacrificed, and their femurs and tibias placed in bone marrow medium (dulbecco’s modified eagle medium, DMEM, with 10% fetal bovine serum, FBS, and 25 ng/mL M-CSF from peprotech). Both ends of the femurs and tibias were cut, and a 27-gauge needle containing phosphate-buffered saline (PBS) was injected into the bone and collected on opposite side of bone containing the bone marrow cells.