Thioacetamide hepatocarcinogenesis.
Thioacetamide (TAA) was administered to inbred male ACI rats for 1 year to determine its hepatocarcinogenicity. The carcinogen was fed at a level of 0.035% in a semipurified diet so that other components could be manipulated. The following groups were used: group I, TAA alone; group II, TAA with riboflavin content at 0.002% (one-third of the daily requirement); group III, TAA plus a supplement of 0.05% crude bovine thyroid; and group IV, TAA, 0.002% riboflavin, and thyroid supplement. All groups demonstrated cirrhosis, neoplastic nodules, and cholangiofibromas to varying degrees. Group IV was invariably the most advanced in all lesions, while group II demonstrated the next most advanced picture of cholangiofibromas. These lesions persisted for 1 year after cessation of the diet. Primary hepatocarcinomas (PHC) were produced by groups I, III, and IV, with the highest number being in group IV. Group II evoked only primary cholangiocarcinomas (PCC). A number of both types of carcinomas transplanted successfully. Thus TAA appears to be a hepatocarcinogen capable of inducing either PHC or PCC, with the tumor type evoked somewhat dependent on the associated diet.[1]References
- Thioacetamide hepatocarcinogenesis. Becker, F.F. J. Natl. Cancer Inst. (1983) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
