Effects of vitamin C on tumor induction by diethylnitrosamine in the respiratory tract of hamsters exposed to cigarette smoke

Harada, Takanori; Kitazawa, Toshiaki; Maita, Keizo; Shirasu, Yasuhiko

doi:10.1016/0304-3835(85)90022-9

Cited by 15 publications

(2 citation statements)

References 4 publications

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“…This indicates that vitamin C injected simultaneously with DMBA accelerated tumor induction such that tumors were founded at an earlier stage than those in the group injected with DMBA alone. This finding was in accordance with the results of previous studies that reported enhancement of the development of laryngeal and tracheal (Harada et al, 1985), bladder (Ito et al, 1984) and forestomach (Imaida et al, 1983) neoplasia in experimental animal groups exposed to different carcinogenic materials combined with vitamin C which suggested the role of vitamin C as promoter of various type of carcinoma (Fukushima et al, 1988). In addition, tumor growth was shown to be considerably increased by vitamin C injected subcutaneously or fed in high concentrations by mouth (Migliozzi, 1977;Maeda et al, 2000).…”

Section: Discussionsupporting

confidence: 92%

Vitamin C Increases the Level of Lactate Dehydrogenase in Rats ‘Oral Squamous Cell Carcinoma

Hadad¹,

Bioinformatics²

2018

JEBAS

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Since the discovery of vitamin C many studies have illustrated its characteristic effect as a tumor prevention agent. Conversely: the extracellular presence of lactate dehydrogenase (LDH) is associated with cell necrosis and tissue breakdown and is therefore considered as a tumor marker. In present study effects of vitamin C on the levels of oral LDH was estimated during the development of squamous oral carcinoma. Histological findings of study revealed changes in the oral tissue of the animals treated with dimethyl benzanthracene (DMBA) alone or DMBA associated with vitamin C such as moderate dysplasia associated with basal cell hyperplasia. Notably: differentiated oral squamous cell carcinoma was observed in the rats belonging to group injected with DMBA after 6 weeks. Otherwise: anaplastic oral carcinoma was observed after 5 weeks in group treated with DMBA and vitamin C. High levels of LDH were detected throughout the induction of the squamous cell carcinoma phases in comparison to the anaplastic phase. These findings demonstrate that the injection of DMBA in association with vitamin C accelerates the induction of anaplastic carcinoma and that these changes are associated with increased LDH levels in the differentiated squamous carcinoma compared with the undifferentiated carcinomas.

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Section: Discussionsupporting

confidence: 92%

Vitamin C Increases the Level of Lactate Dehydrogenase in Rats ‘Oral Squamous Cell Carcinoma

Hadad¹,

Bioinformatics²

2018

JEBAS

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“…Tracheal and nasal cancer induced in hamsters by N-nitrosodiethylamine (DEN) and cigarette smoke ( 19), and lung cancer induced by dimethylnitrosamine (DMN) in mice (40) were all inhibited in animals fed vitamin C. Mammary carcinogenesis by DMBA was not influenced by vitamin C supplements in the drinking water ( 1 ).…”

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confidence: 97%

Update on the Effects of Vitamins A, C, and E and Selenium on Carcinogenesis

Birt¹

1986

Experimental Biology and Medicine

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The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing (i) the effect of vitamin A deficiency, (ii) the effect of excess vitamin A, or (iii) the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A (i) enhanced or inhibited skin tumorigenesis, (ii) inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or (iii) enhanced or did not influence lung carcinogenesis. Vitamin A analogs have (i) enhanced or inhibited skin tumorigenesis, (ii) inhibited salivary gland, mammary, and urinary bladder carcinogenesis, (iii) enhanced tracheal and liver carcinogenesis, and (iv) either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed.Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin. In conclusion, interactions among these vitamins and minerals, other nutrients and other nonnutrient dietary components in cancer prevention should be vigorously pursued, since studies with vitamins A, C, and E and selenium have generally indicated enhancement, as well as inhibition, of carcinogenesis. o

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Effects of vitamins C and E on N‐nitroso compound formation, carcinogenesis, and cancer

Mirvish

1986

Cancer

227

106

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The properties of N-nitroso compounds (NNC) and of vitamins C and E are briefly described. The author reviews the ability of vitamins C and E to inhibit NNC formation in chemical systems, in nitrite-preserved meat, in experimental animals and in humans. Dietary vitamins C and E both produced 30% to 60% inhibitions in most carcinogenesis experiments employing preformed carcinogens. Vitamin C reversed transformation in an in vitro system. Carcinogenicity tests of the vitamins are reviewed (vitamin C can promote bladder carcinogenesis). Intake of fresh fruits and vegetables (which contain vitamin C) is negatively correlated with cancer of the stomach, esophagus, larynx, mouth and cervix. For gastric and esophageal cancer, there is evidence that this association is due to an inhibition of in vivo NNC formation. Vitamin C is apparently not a useful treatment for cancer. The author supports the recommendation that fresh fruit and vegetable intake be increased to lower the risk of cancer.

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Effects of vitamin C on tumor induction by diethylnitrosamine in the respiratory tract of hamsters exposed to cigarette smoke

Cited by 15 publications

References 4 publications

Vitamin C Increases the Level of Lactate Dehydrogenase in Rats ‘Oral Squamous Cell Carcinoma

Vitamin C Increases the Level of Lactate Dehydrogenase in Rats ‘Oral Squamous Cell Carcinoma

Update on the Effects of Vitamins A, C, and E and Selenium on Carcinogenesis

Effects of vitamins C and E on N‐nitroso compound formation, carcinogenesis, and cancer

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