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  3. Standard operating procedures in experimental liver research: thioacetamide model in mice and rats

Standard operating procedures in experimental liver research: thioacetamide model in mice and rats

  • Lab Anim. 2015 Apr;49(1 Suppl):21-9. doi: 10.1177/0023677215573040.
M C Wallace 1,  K Hamesch 2,  M Lunova 2,  Y Kim 3,  R Weiskirchen 4,  P Strnad 5,  S L Friedman 6
Affiliations

Affiliations

  • 1 Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • 2 Department of Internal Medicine III, RWTH University Hospital Aachen, Aachen, Germany.
  • 3 Kyung Hee Medical Center, Seoul, Korea.
  • 4 Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry, RWTH University Hospital Aachen, Aachen, Germany.
  • 5 Department of Internal Medicine III, RWTH University Hospital Aachen, Aachen, Germany Interdisciplinary Center for Clinical Research (IZKF), RWTH University Aachen, Aachen, Germany.
  • 6 Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York, USA scott.friedman@mssm.edu.
PMID: 25835735 DOI: 10.1177/0023677215573040
Abstract

In addition to carbon tetrachloride (CCl4), thioacetamide (TAA) represents a second widely used model for the induction of experimental liver fibrosis, but can also be employed for the development of acute liver failure and liver tumours. While TAA itself is not hepatotoxic, its reactive metabolites covalently bind to proteins and lipids thereby causing oxidative stress and centrilobular necrosis. Compared with CCl4, TAA leads to more periportal infiltrates and more pronounced ductal proliferation. While TAA has been shown to induce liver fibrosis development in several different mouse strains, wide variations in the administration routes, doses and treatment durations have been reported. Therefore, an adoption of a universal standard operating procedure for the administration of TAA is urgently needed. For that purpose, we are presenting here two TAA models (intraperitoneal administration of 150 mg/kg of TAA three times per week for 11 weeks in rats, and TAA administration in drinking water at 300 mg/L for 2-4 months in mice) with which we have had success in reliably and reproducibly developing chronic liver injury and fibrosis.

Keywords

CYP2E1; animal models; cirrhosis; hepatotoxin; liver fibrosis.

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