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Review
. 2023 Apr:99:104093.
doi: 10.1016/j.etap.2023.104093. Epub 2023 Mar 2.

Molecular mechanisms in thioacetamide-induced acute and chronic liver injury models

Devaraj Ezhilarasan  1
Affiliations
Review

Molecular mechanisms in thioacetamide-induced acute and chronic liver injury models

Devaraj Ezhilarasan. Environ Toxicol Pharmacol. 2023 Apr.

Abstract

Thioacetamide (TAA) undergoes bioactivation in the liver by the CYP450 2E1 enzyme, resulting in the formation of TAA-S-oxide and TAA-S-dioxide. TAA-S-dioxide induces oxidative stress via lipid peroxidation of the hepatocellular membrane. A single TAA dose (50-300 mg/kg) administration initiates hepatocellular necrosis around the pericentral region after its covalent binding to macromolecules in the liver. Intermittent TAA administration (150-300 mg/kg, weekly thrice, for 11-16 weeks) activates transforming growth factor (TGF)-β/smad3 downstream signaling in injured hepatocytes, causing hepatic stellate cells (HSCs) to acquire myofibroblast like phenotype. The activated HSCs synthesize a variety of extracellular matrix, leading to liver fibrosis, cirrhosis, and portal hypertension. The TAA induced liver injury varies depending on the animal model, dosage, frequency, and routes of administration. However, TAA induces hepatotoxicity in a reproducible manner, and it is an ideal model to evaluate the antioxidant, cytoprotective, and antifibrotic compounds in experimental animals.

Keywords: Liver fibrosis; Liver necrosis; Oxidative stress; Thioacetamide.

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Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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