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NAC limits the hepatoxicity of APAP by increasing the synthesis of GSH in the liver [39]

Ann Intern Med 92:511511 ODell JR, Zetterman RK, Burnett DA (1986) Centrilobular hepatic fibrosis following acetaminophen-induced hepatic necrosis in an alcoholic

(1) Both these findings on chronic and acute action of AOD 9604 suggested that while enhanced beta(3)-AR expression may have played a role in the chronic action of the compound, beta(3)-AR might not be the sole arbiter in this reaction

However, after a large dose of APAP, the sulfonation reaction becomes saturated and the build-up of NAPQI depletes GSH in the liver, causing further accumulation of NAPQI

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