Abstract: Our previous studies found that the alcoholic extract of the kernels of Fructus Schizandrae (AKS) and its certain components significantly protected against CCl₄ hepatotoxicity in mice. This paper reports the protective action of AKS and schisandrol B (one of the components) against acetaminophen hepatotoxicity in mice.Mice were treated with AKS 0.5g/kg (calculated as raw materials 5g/kg) and schisandrol B 200 mg/kg, separately, 24 hours before ip injection of acetaminophen 400 mg/kg. The number of mice died and depletion of liver glutathione induced by acetaminophen were reduced significantly. Blood acetaminophen concentration of schisandrol B-treated mice was much lower than that of the control mice, whereas the rate of acetaminophen metabolism by liver microsomes from schisandrol B-treated mice was higher than that from control mice. AKS and schisandrol B were shown to be phenobarbital-like inducer of microsomal cytochrome p-450. However, phenobarbital (100 mg/kg) pretreatment was not shown to revent the death of mice and acetaminophen(400 mg/kg ip.) induced depletion of liver glutathione.It appears that the hepato-protective action of AKS and schisandrol B against acetaminophen might be due to induction of a new form of cytochrome p-450 which modified the pathway of acetaminophen metabolism, thereby, decreased the formation of toxic intermediate (s).