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Normally, the excess of ROS in the mitochondria is neutralized by the endogenous antioxidant system which comprises several enzymes and non-enzymatic antioxidants [100] including reduced glutathione (GSH), vitamins C, and E, the Cu/Zn-superoxide dismutase (SOD) in the cytoplasm, and Mn-SOD in the mitochondrial matrix, catalase in the peroxisomes, glutathione peroxidase (GSH-Px), etc

Both alcohol and isoniazid induce CYP2E1 and affect APAP-induced ALI by increasing NAPQI, the hepatotoxic metabolite of APAP, indicating that CYP2E1 may be the major P450 contributing to conversion of APAP to NAPQI (Zand et al., 1993

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