The study was undertaken to determine whether aflatoxin B1 (AFB1)-induced liver tumors in rats produced alpha1-fetoprotein (AFP) and whether the age of the animals would influence such as appearance, a finding suggested by data seen in man. Other liver carcinogens (N-hydroxy-N-2-fluorenylacetamide, N-2-fluorenylacetamide, and diethylnitrosamine) were tested for their ability to induce liver tumors producing AFP. The presence of AFP. The presence of AFP in the serum was determined by double diffusion in agarose and by comparison also by quantitative radioimmunoassay. Using double diffusion, AFP was detected in the majority of tumor-bearing rats that had received either N-2-fluorenylacetamide or N-hydroxy-N-2-fluorenylacetamide. Sera of diethylinitrosamine-treated rats with liver tumors were all positive, whereas sera of rats bearing AFB1-induced tumors were positive in only a few cases. However, all sera of tumor-bearing rats examined had elevated AFP levels by radioimmunoassay. Nonetheless, the average level of AFP in the sera of rats bearing AFB1-induced tumors was considerably lower, compared to the sera of rats with tumors caused by diethylnitrosamine, N-2-fluorenylacetamide, or N-hydroxy-N2-fluorenylacetamide. Rats started on AFB1 when 6 weeks old had more mixed liver tumors with neoplastic hepatocytes and bile ducts and higher AFP levels than did rats started at 26 weeks of age. However, the histological grade of differentiation of inducted tumors did not seem to influence the AFP level.

Aflatoxins↗

PubMed1975

A study of alpha1-fetoprotein levels during exposure to 3'-methyl-4-dimethylaminoazobenzene and its analogs.

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.

Alpha-Globulins↗

PubMed1975

Sequential analysis of transplantable hepatocellular carcinomas.

In a previous study multiple characteristics of chemically induced primary hepatocellular carcinomas were described and examined during the initial transplant generations. The present communication reports on these characteristics in subsequent transplant generations followed over a 2-year period. In almost all instances the growth rate, morphology, chromosome composition, and plasma protein and alpha-fetoprotein synthesis of individual tumors have remained relatively constant. However, one spontaneous subline of a diploid tumor demonstrated a sudden extensive rearrangement of its chromosomes simultaneous with a significant acceleration of growth rate. Despite karyotypic evolution, it retained the functional characteristics of diploid tumors, producing no plasma protein or alpha-fetoprotein.

2-Acetylaminofluorene↗

PubMed1974