ABSTRACT
A previous study demonstrated that cells of transplantable hepatocellular carcinomas were agglutinated by the plant lectin concanavalin A, while normal hepatocytes were not. In the present experiments, 95% or more of cells obtained from primary hepatocellular carcinomas which resulted from exposure of rats to N-2-fluorenylacetamide were agglutinated by this lectin. Exposure to this carcinogen also produces grossly visible foci of morphologically and biochemically altered hepatocytes which have been termed hepatic (hyperplastic; premalignant, neoplastic) nodules. Although these hepatocyte aggregates are generally accepted as precursors of the hepatocellular carcinomas, no agglutination was detected when their cells were exposed to concanavalin A. These results indicate that concanavalin A agglutinability is not acquired as a result of tumor transplantation. Furthermore, they suggest that significant alterations must occur in the cells of hepatic nodules prior to the manifestation of malignant behavior.
Subject(s)
Agglutination , Carcinoma, Hepatocellular/pathology , Concanavalin A/pharmacology , Liver Neoplasms/pathology , Precancerous Conditions/pathology , 2-Acetylaminofluorene , Animals , Carcinoma, Hepatocellular/chemically induced , Liver Neoplasms/chemically induced , Male , Neoplasms, Experimental/chemically induced , Neoplasms, Experimental/pathology , Rats , Rats, Inbred ACIABSTRACT
The serum concentration of alpha1-fetoprotein (alpha1F) was determined in rats following exposure to the hepatocarcinogen, 3'-methyl-4-dimethylaminoazobenzene, and its analogs. Small quantities of the carcinogen caused a rapid and significant elevation of alpha1F. Neither 2-methyl-4-dimethylaminoazobenzene nor p-aminoazobenzene resulted in any elevation of alpha1F. Further, under circumstances wherein 2-methyl-4-dimeth-laminoazobenzene is reported to become carcinogenic, i.e., when administered at the time of 70 percent hepatectomy, neither elevation of alpha1F nor histological alteration of the liver was noted. The increase in alpha1F after 3'-methyl-4-dimethylaminoazobenzene exposure is the result of a highly selective interaction. The possible contribution of hepatocyte mitosis to the elecation of alpha1F seen during chemical carcinogenesis is emphasized.
