Influence of repeated liver regeneration on hepatic carcinogenesis by diethylnitrosamine in mice

Poound, A. W.; McGuire, Lloyd

doi:10.1038/bjc.1978.89

Cited by 55 publications

(9 citation statements)

References 16 publications

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“…However, weekly treatment of CCl 4 enhanced AFB 1 -induced enzyme altered foci several fold both in area and volume. The present results are thus in agreement with previous data of other investigators who demonstrated that repeated CCl 4 treatment of various rodent species including rats enhanced nitrosamine-initiated hepatocytes to form enzyme altered foci and nodules (Pound and McGuire, 1978;Dragani et al, 1986; Ta n a k a et Columbano et al, 1990;Zalatnai et al, 1991;Cho and Jang, 1993). In earlier studies, GGT was widely used as an enzyme marker for detecting the production of enzyme altered foci in rodent hepatocarcinogenesis (Kalengayi et al, 1975; C a y a m a et Pitot et al, 1978;Columbano e t al., 1987).…”

Section: Discussionsupporting

confidence: 93%

Enhancement of aflatoxin B1-induced enzyme altered hepatic foci in rats by treatment with carbon tetrachloride

Qin

Ning²,

Su³

et al. 1998

Exp Mol Med

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The effect of carbon tetrachloride (CC1 4 ) on aflatoxin B 1 (AFB 1 )-induced enzyme altered hepatic foci has been examined in young male Fischer rats given AIN-76A diet. A single i.p. dose of AFB 1 (0.2 mg/kg body wt) was given to rats 24 h after partial hepatectomy. Two weeks later, CCl 4 (0.8 ml/kg body wt) was injected i.p. once a week for 9 weeks. Animals were sacrificed 24 h after the last dose of CC1 4 and glutathione S-transferase placental form (GST-P) and -glutamyl transpeptidase (GGT) positive hepatic foci were analyzed by immunohistochemical and histochemical methods, respectively. Ten weeks after A F B 1 dosing, treatment with CCl 4 increased the number of AFB 1 -induced enzyme altered foci several fold and produced a ten to twenty-fold increase in area and volume. GST-P was more sensitive than GGT in detecting AFB 1 -i n d u c e d enzyme altered foci. Treatment with AFB 1 or CCl 4 produced mild hepatic fibrosis in zones 1 and 3 r e s p e c t i v e l y, whereas both treatments produced severe fibrosis in zones 1 to 3 areas. Tr e a t -ment with CCl 4 after AFB 1 dosing lowered hepatic GSH levels by 20% and increased lipid peroxidation by 40%. It appears that CCl 4 , by being an effective enhancer of AFB 1 -induced enzyme altered hepatic foci in the rat, may mimic cirrhosis observed in human hepatocellular carcinoma.

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Section: Discussionsupporting

confidence: 93%

Enhancement of aflatoxin B1-induced enzyme altered hepatic foci in rats by treatment with carbon tetrachloride

Qin

Ning²,

Su³

et al. 1998

Exp Mol Med

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“…Partial hepatectomny after a dose of radiation inarginally increased hepatoma yields (Haran-Ghera et al, 1962). Repeated doses of CC14 at 5-week intervals, starting 5 weeks after a dose of DEN to mice, greatly enhanced the yields of tumours (Pound and McGuire, 1978). The relationship of "focal proliferations" to the "hyperplastic nodules" and similar lesions described by other authors is not clear; size alone appears to be one criterion.…”

Section: Discussionmentioning

confidence: 90%

Repeated partial hepatectomy as a promoting stimulus for carcinogenic response of liver to nitrosamines in rats

Pound¹,

McGuire²

1978

Br J Cancer

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Partial hepatectomy 24 h before a single i.p. dose of dimethylnitrosamine, diethylnitrosamine or ethylmethylnitrosamine increased the carcinogenic response in the liver of rats as determined by the number of tumours and the number of "focal proliferations" produced. Secondly, in rats given a single i.p. dose of diethylnitrosamine, 3 partial hepatectomies 5, 10 and 15 weeks after dosing the animals increased the carcinogenic response in the liver. The stimulus of repeated partial hepatectomy therefore appears to act as a "promoting agent" for liver carcinogenesis, that is if the single dose of diethylnitrosamine is regarded as an "initiating agent" in the terms of the two-stage hypothesis. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4

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“…Even though the role played in tumor promotion by both quantity and quality of dietary fat appears to be complex, it was of interest to find in the present study that there is no correlation between efficacy of the promotion and degree of stimulation of liver cells proliferation with CD diets containing different amounts of fat. Enhanced liver cell proliferation induced by a partial hepatectomy or a necrogenic dose of carbon tetrachloride has been shown to accelerate the development of liver tumors in rats or mice initiated with a variety of carcinogens (19)(20)(21)(22). However, our findings suggest that the general properties of enhanced cell proliferation per se are not the sole factors in determining the efficacy of tumor promotion in the liver and that other factors must be involved.…”

Section: Discussionmentioning

confidence: 54%

Modulation of Tumor Promotion in Liver Carcinogenesis

Satoh¹,

Abanobi²,

Lombardi³

1983

Environmental Health Perspectives

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Earlier, we demonstrated that feeding to rats a diet devoid of choline, a lipotropic factor, markedly enhances hepatoma induction by several chemical carcinogens, and that the diet acts as a strong promoter of the evolution of initiated cells to foci of altered hepatocytes. The ability of several factors to modulate the action of the choline-devoid (CD) diet as a promoter was investigated by quantitating the foci of y-glutamyl transpeptidase-positive hepatocytes developed in rats exposed to a single injection of diethylnitrosamine. Addition to the diet of phenobarbital (PHB) resulted in a promoting action stronger than those of the CD diet or of PHB alone. Two other barbiturates, amobarbital (AMB) and pentobarbital (PTB) exerted an effect similar to that of PHB, while barbituric acid (BA) had no effect. In other studies, lowering the fat content of the CD diet reduced its efficacy as a promotor, while the addition of a hypolipidemic agent, BR931, 4-chloro-642,3 xylidino)-2-pyrimidinylthio (N-p-hydroxy-ethyl)acetamide, completely abolished the promoting action of the CD diet. In rats not exposed to carcinogen, feeding the CD diet caused a marked enhancement of liver DNA synthesis and of cell proliferation. Inclusion of PHB, PTB or AMB in the CD diet inhibited these effects, while BA exerted no inhibition. The increased rate of DNA synthesis and cell proliferation in the liver were not affected by the level of fat in the CD diet. These results suggest that beside a stimulation of liver cell proliferation, other factor(s) determine the efficacy with which a CD diet exerts its promoting action.

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Influence of repeated liver regeneration on hepatic carcinogenesis by diethylnitrosamine in mice

Cited by 55 publications

References 16 publications

Enhancement of aflatoxin B1-induced enzyme altered hepatic foci in rats by treatment with carbon tetrachloride

Enhancement of aflatoxin B1-induced enzyme altered hepatic foci in rats by treatment with carbon tetrachloride

Repeated partial hepatectomy as a promoting stimulus for carcinogenic response of liver to nitrosamines in rats

Modulation of Tumor Promotion in Liver Carcinogenesis

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