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Reduction and enhancement by phenobarbital of hepatocarcinogenesis induced in the rat by 2-acetylaminofluorene.
Summary The effects of dietary phenobarbital on hepatocarcinogenesis in rats fed 2-acetylaminofluorene (AAF) were studied. The simultaneous feeding of AAF and phenobarbital reduced theExpand
Comparative enhancing effects of phenobarbital, amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.
The results show that the sequential treatment technique readily distinguishes among substances differing in enhancing ability and should prove useful in screening additional substances for this activity, and shows that Phenobarbital and DDT selectively increased the incidence of highly differentiated tumors throughout most of the experiment. Expand
Enhancing effects of phenobarbitone and butylated hydroxytoluene on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.
The results suggest that the dissimilar tumorigenic-enhancing abilities of BHT and phenobarbitone may result from differences in the effects of these agents on biochemical processes related to liver growth. Expand
Early appearance of histochemically altered hepatocyte foci and liver tumors in female rats treated with carcinogens one day after birth.
The results suggest that the treatment protocol used in this study may increase the utility of the liver tumorigenesis model as a broadly applicable in vitro system for the rapid detection of tumorigenic potential in environmental contaminants. Expand
The radioprotector WR1065 reduces radiation-induced mutations at the hypoxanthine-guanine phosphoribosyl transferase locus in V79 cells.
Although a segment of radiation-induced damage leading to reproductive death cannot be modulated through the postirradiation action of WR1065, processes leading to the fixation of gross genetic damage and mutation induction in surviving cells can be effectively altered and interfered with leading to a marked reduction in mutation frequency. Expand
Effects of varying the exposure to phenobarbital on its enhancement of 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.
Results indicated that prolonged exposure to phenobarbital was required for tumorigenic enhancement and the tumorigenIC lesion produced by AAF was relatively stable, and its expression could be enhanced by phenobar bital long after the cessation of AAF treatment. Expand
Systematic oscillations in metabolic activity in rat liver and in hepatomas. I. Morris hepatoma No. 7793.
Environmentally induced changes in rat liver were used to determine the capability of a minimal deviation hepatoma (Morris hepatoma 7793) to respond to regulatory influences and it was noted that at dietary protein levels that depressed enzyme activity in host liver, enzyme activities in the hepatomas attained values 10–100 times higher than those of livers in the same animals. Expand
Characterization of histochemically detectable altered hepatocyte foci and their relationship to hepatic tumorigenesis in rats treated once with diethylnitrosamine or benzo(a)pyrene within one day
It is suggested that foci emerge as the result of a specific set of cellular changes solely inducible by carcinogenic stimuli, but the foci do not evolve through progressively more deviated forms into tumors. Expand