Vitamins carcinogenesis

Mirvish (53,54) discovered that vitamin C could inhibit ni-trosation reactions. The purely chemical interaction of ascorbic acid with nitrite has been studied for theoretical reasons and because of its importance in the preservation of foods. This interaction has received increased attention for minimizing the presence of nitrosamines and nitrosamides in the environment, and especially in foods. We have studied the relationship in gastric carcinogenesis between high levels of nitrite, including pickling, and of vitamin C as a protective and inhibiting element. 

In addition, there is now epidemiological evidence that dietary antioxidants, such as vitamins A, C, D and E, phytic acid, and protease inhibitors can prevent carcinogenesis, including that of the gastrointestinal (GI) tract (Graf and Eaton, 1990 Block, 1991 Malone, 1991 Troll, 1991 Weisburger, 1991). 

Gerster, H. 1995. Carotene, vitamin E and vitamin C in different stages of experimental carcinogenesis. EurJ Clin Nutr 49 155-168. 

The consumption of a mixture of phenolic compounds presented in apple or purple grape juice inhibited mammary carcinogenesis in 7,12-dimethylbenzo[a]anthracene (DMBA) treated rats (Liu and others 2005 Jung and others 2006). However, the individual antioxidants of these foods studied in clinical trials, including (3-carotene, vitamin C, and vitamin E, do not appear to have consistent preventive effects comparable to the observed health benefits of diets rich in fruits and vegetables, suggesting that natural phytochemicals in fresh fruits and vegetables could be more effective than a dietary supplement. 

M. Fenech, C. Aitken, and J. Rinaldi, Folate, Vitamin B12, Homocysteine Status and DNA Damage in Young Australian Adults, Carcinogenesis 19 (1998) 1163-71. 

Fenech, M., Baghurst, P., Luderer, W., Turner, J., Record, S., Ceppi, M., and Bonassi, S. (2005). Low intake of calcium, folate, nicotinic acid, vitamin E, retinol, beta-carotene and high intake of pantothenic acid, biotin and riboflavin are significantly associated with increased genome instability—Results from a dietary intake and micronucleus index survey in South Australia. Carcinogenesis 26, 991-999. 

Because vitamin A regulates epithelial cell differentiation and proliferation, there has been considerable interest in the apparent ability of retinol and related compounds to interfere with carcinogenesis. Vitamin A deficiency in humans enhances susceptibility to carcinogenesis. 

Water-soluble vitamins and co-factors also appear to elicit an effect on xenobiotic metabolism. Ascorbic acid has been shown to inhibit chemically induced chemical carcinogenesis in test systems (Shamberger, ( ). When diets are deficient in choline, the animals appear to become much more susceptible to chemically-... 

Fat-soluble vitamins, in addition to their antioxidative effects on lipids, appear to exert a general protective effect in animals. Vitamin A and beta-carotenes protect lab animals from toxicity of citral, cyclophosphamide and some hydrocarbons (Seifter et al, (A2.) In related but independent studies, it was observed that high levels of vitamin A inhibit tumorogenesis and that low levels of vitamin A appear to enhance tumorogenesis (Baird, (1 ). vitamin E inhibited chemically-induced carcinogenesis in test systems (Shamberger, ) and also reduced the susceptibility of rats to cigarette smoke (Chow,... 

Vitamins. The laboratory evidence suggests that vitamin A itself and many of the retinoids are able to suppress chemically induced carcinogenesis. The epidemiological evidence is sufficient to suggest that foods rich in carotenes or vitamin A are associated with a reduced risk of cancer. 

There have been several epidemiological and several case reports inversely relating ascorbic acid intake from food to human cancer mortality. These studies are interesting, but may be confounded with the fact that the same ascorbic acid containing foods, namely fruits and vegetables, also contain large amounts of vitamin A and fiber. Both vitamin A and fiber have been inversely related to human cancer mortality and have been shown to inhibit several types of chemically-induced carcinogenesis in animals. Therefore, the possible anti cancer effect of ascorbic acid may be due to other factors. 

While there are no epidemiologic data available on lipotropic factors and colon cancer in human populations, results of animal studies suggest a possible role for this class of nutrients (choline, methionine, vitamin and folate) in colon carcinogenesis (69). Table XVI lists results typical of those observed when rats are fed a diet high in fat, low in lipotropes and exposed to a colon carcinogen. 

There is little in the literature relative to vitamin A and colon cancer in human populations. Experimental animal studies, however, strongly suggest that vitamin A deficiency may have a role in this type of cancer. We have shown that a deficiency of vitamin A increased DMH-induced tumors and shortened the lag time for induction, compared to normally supplemented controls (72). More recently (73) we have confirmed a protective role for vitamin A in colon carcinogenesis (Table XVII). Furthermore, we have shown (74) that vitamin A deficiency can result in colon tumors in rats given aflatoxin (AFB ) which is normally a liver carcinogen (Table XVIII). The colon tumors associated with the hepatocarcinogen AFB.. appear to be a result of differences in metabolism and binding of AFB or its metabolite ) to colon DNA under conditions of vitamin A deficiency (75). 

Sugiyama M, Ando A, Ogura R. 1989. Effect of vitamin E on survival, glutathione reductase and formation of chromium(V) in Chinese hamster V-79 cells treated with sodium chromate(VI). Carcinogenesis 10 737-741. 

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