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Recent investigations on mechanism of carcinogenesis have demonstrated important quantitative relationships between the induction of neoplasia, the molecular dose of promutagenic DNA adducts and their efficiency for causing base-pair mismatch, and the extent of cell proliferation in target organ. These factors are involved in the multistage process of(More)
Chronic exposure to the hepatocellular carcinogen diethylnitrosamine (DEN) causes a dose-dependent accumulation of the promutagenic DNA adduct O4-ethyldeoxythymidine in hepatocytes and increases in the number of initiated hepatocytes as indicated by gamma-glutamyl transpeptidase positive foci. Initiation is thought to be dependent on the quantity of(More)
Incorporation of the molecular dosimetry of DNA adducts is being proposed as a means for placing quantitative risk assessment on a stronger scientific basis. While this is likely to be an improvement over straight mathematical extrapolation, we believe that a more holistic approach that incorporates even more biology is needed. Therefore, we have begun to(More)
The concentration of DNA adducts in specific hepatic cell types has been determined in F344 rats fed 0.02% 2-acetylaminofluorene (AAF) for 28 days followed by control diet for an additional 28 days. In animals killed at 28 days of AAF feeding, the major DNA adduct, N-(deoxyguanosin-8-yl)-2-aminofluorene, was present in each cell type in the order:(More)
Hepatocyte initiation, as indexed by growth-selected gamma-glutamyl transferase-positive foci, was measured during continuous exposure to diethylnitrosamine (DEN) at concentrations used in previous DEN bioassay, DNA adduct, and cell replication studies. Hepatocyte initiation increased in a dose- and lobe-specific manner. The efficiency of DEN as an(More)
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