Thioacetamide (TAA) is an indirect hepatotoxin and causes parenchymal cell necrosis. Thioacetamide requires metabolic activation by microsomal CYP2E1 to thioacetamide-S-oxide initially and then to thioacetamide-S-dioxide, which is a highly reactive metabolite, and its reactive metabolites covalently bind to proteins and lipids thereby causing oxidative stress and centrilobular necrosis. Thioacetamide can induce chronic liver fibrosis, encephalopathy and other events model[2].In Vitro:Thioacetamide (TAA; 0-10000 μM; 24 h; WB-F344 cells) has cytotoxicity in a concentration-dependent manner.
Thioacetamide (TAA; 1000 and 10000 μM; 0-24 h; WB-F344 cells) has differentially-expressed genes in the early phases at low (1000 μM) and high (10000 μM) concentrations.
In Vivo:Thioacetamide (TAA; 100 mg/kg; i.p.; three times weekly) can induce chronic liver fibrosis in male ICR mice[2].
Thioacetamide (200-1200 mg/kg; i.p.; once) induces hepatic encephalopathy model in C57BL/6 mice.