Effect of dietary selenium levels on methylbenzylnitrosamine-induced esophageal cancer in rats

Nauss, Kathleen M.; Bueche, Doug; Soule, N.; Fu, Penelope; Yew, Kristine; Newberne, Paul M.

doi:10.1016/0304-3835(86)90107-2

Cited by 13 publications

(5 citation statements)

References 9 publications

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“…Fong and co-workers (26) reported that zinc deficiency can significantly increase the NMBA-induced esophageal tumors with the carcinogen dose of 4 mg/kg each week for 12 weeks by gavage. In addition, the present results are consistent with the findings of Nauss and colleagues (11), who found no effects of dietary selenium levels on NMBA-induced tumorigenesis. In their study, the total carcinogen dosages were 40 mg/kg, almost the same as in the present study, but the observation time was as long as 35 weeks.…”

Section: Discussionsupporting

confidence: 95%

“…The present results are consistent with the findings of Nauss and others (11), who found no effects of dietary selenium levels on NMBA-induced tumorigenesis, but are contrary to those of Bodgen and co-workers (10), who found that selenium can significantly decrease NMBA-induced esophageal tumors. Possible explanations for this discrepancy are the limited number of animals in each treated group (9 rats) in the study of Bogden and co-workers and the growth retardation effect in the selenium-supplemented group over the last two weeks of the experiment, because calorie restriction has been shown to be tumor protective (27).…”

Section: Discussionsupporting

confidence: 52%

“…The results of the only two previous studies in this field are contradictory. Bogden and colleagues (10) reported decreased NMBA-induced esophageal tumor incidence in selenium-treated rats, but Nauss and others (11) reported that neither selenium deficiency nor selenium supplementation had any effect on esophageal tumorigenesis induced by NMBA in rats. When given orally, NMBA can induce forestomach tumors in mice, but no studies on the effects of selenium on this animal model have been reported.…”

Section: Introductionmentioning

confidence: 96%

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Lack of effects of selenium onN‐nitrosomethylbenzylamine‐induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice

Han²,

Wild³

et al. 1992

Nutrition and Cancer

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The effects of dietary selenium deficiency and excess on N-nitrosomethylbenzylamine-(NMBA) induced esophageal neoplasia in rats and forestomach tumors in mice and the effects of dietary selenium on DNA adduct formation and on the activities of DNA adduct-repairing enzyme and oncogene expression in rat esophagus were investigated. The esophageal and forestomach tumors were induced by administration of NMBA by gavage with a total dose of 39 mg/kg body wt in rats and 12 mg/kg body wt in mice. Neither selenium dietary deficiency (Se < 0.02 ppm) nor selenium excess (2.0 ppm) showed any significant effect on the incidence of tumors or number of tumors per tumor-bearing animal. For the DNA adduct formation studies, rats were given a dose of NMBA intraperitoneally after six weeks on the different selenium-containing diets. No significant difference in the amount of the DNA adduct O6-methyldeoxyguanosine was found among the different selenium-treated groups. In a parallel group of rats that did not receive NMBA, the levels of esophageal O6-methyldeoxyguanosine DNA methyltransferase were not significantly altered by dietary selenium levels. The c-myc oncogene expression in rat esophagus was induced by the administration of NMBA (3 mg/kg body wt) by gavage once a week for eight weeks. Dietary selenium did not show any effects on its expression. On the basis of the results of these studies, dietary selenium has no effects in the NMBA-induced tumor model.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 96%

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Lack of effects of selenium onN‐nitrosomethylbenzylamine‐induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice

Han²,

Wild³

et al. 1992

Nutrition and Cancer

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“…14) In a recent review, Steinmetz and Potter 15) reported that 10 of 11 epidemiological case-control studies found a significant inverse relationship between the intake of fresh fruits or vegetables and esophageal cancer risk. In animal models for esophageal cancer, diallyl sulfide 16,17) in garlic, derivatives of cruciferous vegetable isothiocyanates, 18,19) green and black tea, 8,20) selenium, 21) ellagic acid, 22) protease inhibitors 23) and diosmin and hesperidin 24) have been reported to inhibit esophageal carcinogenesis. Fig.…”

Section: Introductionmentioning

confidence: 99%

Suppression of N‐Nitrosomethylbenzylamine‐induced Rat Esophageal Tumorigenesis by Dietary Feeding of 1′‐Acetoxychavicol Acetate

Kawabata

Tanaka

Yamamoto

et al. 2000

Japanese Journal of Cancer Research

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The modifying effects of 1′ ′ ′ ′-acetoxychavicol acetate (ACA) on N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis were investigated in male F344 rats. At 5 weeks of age, all test animals, except those given the test chemical alone, and the control rats received s.c. injections of NMBA (0.5 mg/kg body weight/injection, three times per week) for 5 weeks. At the termination of the study (20 weeks), 75% of rats treated with NMBA alone had esophageal neoplasms (papillomas). However, the groups given a dose of 500 ppm ACA during the initiation phase developed a significantly reduced incidence of tumors (29%; P < < < <0.01). Exposure to ACA (500 ppm) during the post-initiation phase also decreased the frequency of the tumors (38%; P < < < <0.05). A reduction of the incidence of preneoplastic lesions (hyperplasia or dysplasia) was obtained when ACA was administered in the initiation phase (P < < < <0.01). Cell proliferation in the esophageal epithelium, determined by assay of proliferating cell nuclear antigen (PCNA), was lowered by ACA (P < < < <0.05). Blood polyamine contents in rats given NMBA and the test compound were also smaller than those of rats given the carcinogen (P < < < <0.05). These findings suggest that dietary ACA is effective in inhibiting the development of esophageal tumors by NMBA when given during the initiation or post-initiation phase, and such inhibition is related to suppression of cell proliferation in the esophageal epithelium.

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“…Furthermore, diets high in fresh fruit and vegetables are consistently associated with reduced risk for esophageal cancer. 6,7) Using animal models for esophageal cancer, diallyl sulfide in garlic 8,9) derivatives of cruciferous vegetable isothiocyanates, 10,11) green and black tea, 12,13) selenium, 14) ellagic acid, 15) protease inhibitors 16) and 1′-acetoxychavicol acetate 17) have been reported to inhibit esophageal carcinogenesis by N-nitrosomethylbenzylamine (NMBA). 18) Recently, diosmin and hesperidin were also reported to inhibit esophageal carcinogenesis by N-methyl-N-amylnitrosamine (MNAN).…”

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confidence: 99%

Chemopreventive Effect of Curcumin on N‐Nitrosomethylbenzylamine‐induced Esophageal Carcinogenesis in Rats

Ushida

Sugie

Kawabata

et al. 2000

Japanese Journal of Cancer Research

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Modifying effects of curcumin (derived from the rhizome of Curcuma longa L.) during the initiation or post-initiation phase of N-nitrosomethylbenzylamine (NMBA)-induced esophageal carcinogenesis were investigated in male F344 rats. Five-week-old rats were divided into 5 groups, and groups 1, 2 and 3 were given intraperitoneal injections of NMBA (0.5 mg/kg body weight/injection 15 times) for 5 weeks from 7 weeks old to induce esophageal neoplasms. Groups 2 and 3 were fed the diet containing 500 ppm curcumin during the initiation and post-initiation phases, respectively. Group 4 was given the diet containing curcumin throughout the experiment, and group 5 was kept on the basal diet alone and served as an untreated control. Incidence and multiplicity of esophageal neoplasms of group 1 (NMBA alone) were 66.7% and 0.83 ± ± ± ±0.70, respectively. Those of groups 2 and 3 were significantly less than those of group 1 (39.3%, 0.46 ± ± ± ±0.64, P < < < <0.05; 33.3%, 0.36 ± ± ± ±0.56, P < < < <0.05, respectively). Furthermore, the incidence and multiplicity of esophageal preneoplastic lesions (moderate or severe epithelial dysplasia) of group 2 (57.1%, 0.61 ± ± ± ±0.57; 40%, 0.29 ± ± ± ±0.46) or 3 (56.7%, 0.67 ± ± ± ±0.66; 23.3%, 0.23 ± ± ± ±0.43) were less than those of group 1 (100%, 1.67 ± ± ± ±0.70; 70.8%, 0.92 ± ± ± ±0.72) (P < < < <0.05). In this experiment, feeding of curcumin significantly decreased the expression of cell proliferation biomarkers (5-bromo-2′ ′ ′ ′-deoxyuridine labeling index) in the non-lesional esophageal epithelium (P < < < <0.01). These findings indicate that curcumin inhibits NMBA-induced esophageal carcinogenesis when given during the post initiation as well as initiation phase. This inhibition may be related to suppression of the increased cell proliferation induced by NMBA in the esophageal epithelium.

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Effect of dietary selenium levels on methylbenzylnitrosamine-induced esophageal cancer in rats

Cited by 13 publications

References 9 publications

Lack of effects of selenium onN‐nitrosomethylbenzylamine‐induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice

Lack of effects of selenium onN‐nitrosomethylbenzylamine‐induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice

Suppression of N‐Nitrosomethylbenzylamine‐induced Rat Esophageal Tumorigenesis by Dietary Feeding of 1′‐Acetoxychavicol Acetate

Chemopreventive Effect of Curcumin on N‐Nitrosomethylbenzylamine‐induced Esophageal Carcinogenesis in Rats

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