Comparative Prevalence, Multiplicity, and Progression of Spontaneous and Vinyl Carbamate-Induced Liver Lesions in Five Strains of Male Mice
Open Access
- 1 August 2002
- journal article
- research article
- Published by SAGE Publications in Toxicologic Pathology
- Vol. 30 (5) , 599-605
- https://doi.org/10.1080/01926230290105776
Abstract
The overall and age-specific prevalences and multiplicities of spontaneous and chemically induced hepatocellular neoplasia were compared among male B6D2F1, B6C3F1, C3H (C3H/HeNCrl MTV-), B6CF1, and C57BL/6 (C57BL/6NCrl) mice following a single intraperitoneal injection of 0.03 μM vinyl carbamate (VC)/g body weight or vehicle alone at 15 days of age. Additional groups of B6C3F1, C3H, and C57BL/6 males received 0.15 μM VC/g body weight at 15 days of age. For male B6D2F1, B6C3F1, C3H, B6CF1, and C57BL/6 mice, the estimated overall prevalences (and multiplicities) of hepatocellular adenomas or carcinomas in vehicle controls were 14.1% (0.19), 12.3% (0.15), 8.2% (0.10), 7.2% (0.09), and 2.4% (0.02), respectively. The analogous estimates in the low-dose group were 59.2% (1.19), 72.9% (4.07), 48.6% (1.99), 22.8% (0.29), and 43.9% (0.82). Analogous estimates for B6C3F1, C3H, and C57BL/6 mice in the high-dose group were 45.3% (4.29), 59.7% (6.63), and 46.8% (1.74), respectively. Age-specific multiplicity estimates suggested a progression from altered hepatocellular foci (AHF) to hepatocellular neoplasms. Further evidence of progression was provided by the temporal occurrence of hepatocellular adenomas before carcinomas, and the apparent origination of carcinomas within adenomas. Pulmonary metastases were observed in many of the mice with hepatocellular carcinomas. These findings confirm previous observations of strain differences in liver neoplasm response, suggest a progressive development from AHF to adenomas, and ultimately to carcinomas, and show sensitivity to VC-induced hepatocarcinogenesi s in all 5 strains.Keywords
This publication has 19 references indexed in Scilit:
- The Contribution of the Mouse in Hazard Identification StudiesToxicologic Pathology, 1996
- A Critical Appraisal of the Value of the Mouse Cancer Bioassay in Safety AssessmentToxicologic Pathology, 1996
- Hepatocarcinogenicity of chlordane in B6C3F1 and B6D2F1 male mice: evidence for regression in B6C3F1 mice and carcinogenesis independent of ras proto-oncogene activationCarcinogenesis: Integrative Cancer Research, 1995
- Comparative analysis of the methylation status of the 5′ flanking region of Ha-ras in B6C3F1, C3H/He and C57BL/6 mouse liverCancer Letters, 1993
- Enzymic oxidation of ethyl carbamate to vinyl carbamate and its role as an intermediate in the formation of 1,N6-ethenoadenosineChemical Research in Toxicology, 1991
- Mutational activation of the c-Ha-ras gene in liver tumors of different rodent strains: correlation with susceptibility to hepatocarcinogenesis.Proceedings of the National Academy of Sciences, 1991
- Genetic Control of Carcinogenesis in Experimental AnimalsPublished by S. Karger AG ,1990
- Logistic regression analysis of incidental-tumor data from animal carcinogenicity experimentsFundamental and Applied Toxicology, 1986
- Preneoplastic and neoplastic progression during hepatocarcinogenesis in mice injected with diethylnitrosamine in infancy.Environmental Health Perspectives, 1983
- Comparative genotoxicity studies of ethyl carbamate and related chemicals: further support for vinyl carbamate as a proximate carcinogenic metaboliteCarcinogenesis: Integrative Cancer Research, 1982