NAPQI is a toxic intermediate is formed by in small amounts by metabolism of acetaminophen. Depletion of hepatic glutathione stores by NAPQI leads to acute APAP toxicity and acute liver injury.
cassdawgAlso relevant to the question: the CYP450 pathway is what turns acetaminophen into NAPQI, and chronic alcohol abuse is one of the inducers for the CYP pathway so it increases NAPQI production. Chronic alcohol abuse itself also depletes glutathione, increasing propensity for toxicity when acetaminophen is introduced. +3
specialist_jellomy probably stupid thought process was : treatment of acetaminophen toxicity is N acetyl cystine which regenerates gluathione. so toxicity will be coz of dec glutathione. +17
fatboyslim@speciliast_jello your thought process is absolutely right. You are not stupid+
fahad_gondal@agraham416 because the toxicity is being caused by the acetaminophen and not the alcohol, the stem doesn't mention anything about an acute alcohol overdose but does say he took a lot like 18 tablets in 3 days thats like 9g of acetaminophen but if the stem had instead said it was an acute alcoholic episode that caused all these symptoms we could say NADH increase was the answer but then again decreased NAD+ would also be an answer because the metabolism of ethanol consumes NAD+ to yield NADH so if 1 of them goes up the other must go down and vice versa so the question wouldve been done and styled differenttly with alternative options+
NAPQI is a toxic intermediate is formed by in small amounts by metabolism of acetaminophen. Depletion of hepatic glutathione stores by NAPQI leads to acute APAP(?) toxicity and acute liver injury.
submitted by โergogenic22(401)
NAPQI is a toxic intermediate is formed by in small amounts by metabolism of acetaminophen. Depletion of hepatic glutathione stores by NAPQI leads to acute APAP toxicity and acute liver injury.