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Toxity
Oral, mouse: LD50 = 338 mg/kg; Oral, rat: LD50 = 1944 mg/kg. Acetaminophen is metabolized primarily in the liver, in which a lot of it is converted to inactive compounds by conjugation with glucuronic acid and, to a lesser extent, sulfuric acid. Conjugates are subsequently excreted from the kidneys. Just a small part is excreted in unchanged in urine or oxidized through the hepatic cytochrome P450 enzyme system (CYP2E1). Metabolism via CYP2E1 creates a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). The poisonous effects of acetaminophen are because of NAPQI, maybe not acetaminophen itself nor some of the main metabolites. At therapeutic dosages, NAPQI reacts with the sulfhydryl group of glutathione to generate a non-toxic conjugate that’s excreted by the kidneys. High levels of acetaminophen can cause glutathione depletion, accumulation of NAPQI and hepatic necrosis. The maximum daily dose of acetaminophen is 4 g. Liver failure was seen at doses as low as 6 grams every day. Therefore, the maximum daily and only dose of acetaminophen is presently being examined in a few nations. N-acetyl-cysteine, a precursor of glutathione, could be administered in case of acetaminophen toxicity.
Paracetamol Interactions
Inform your doctor about all the medications you take includingPrescription drugs and non-prescription drugs, vitamins, and herbalNutritional supplements. Especially tell your health care provider if you choose:
- ACETAMINOPHEN\/ISONIAZID
- ACETAMINOPHEN\/SULFINPYRAZONE