Abstract
Although selenium was once considered to be a toxic, undesirable and carcinogenic element, it is now recognized as an essential element with anticarcinogenic properties. Epidemiological studies in the United States have shown an inverse relationship between selenium intake and certain forms of cancer in humans, but other factors must be considered since cancer is not higher in people living in selenium-deficient areas of the world (Finland, New Zealand, and Keshan disease area, China). Under most dietary conditions, selenium has been shown to reduce the spontaneous mammary tumor incidence in an inbred strain of mice. In general, selenium will counteract to various degrees, the chemical carcinogens used to produce lesions of the skin [coaltar, 3-methylcholanthrene, α-pyrene, and 7,12 dimethylbenz(a) anthracene (DMBA)], liver (3-methyl-4-dimethyl-aminoazobenzene, aflatoxin B 1, and 2-acetylaminofluorene), mammary gland (DMBA and N-methyl-N-nitrosurea), and intestinal tract [1,2-dimethylhydrazine,bis(2-oxopropyl) nitrosamine, and azoxymethane]. Dietary factors, such as fat, will modify the protective effects of selenium. High dietary unsaturated fats, for example, markedly increase the mammary tumors in rats treated with DMBA, and selenium will reduce the tumor incidence but not to the level of rats fed a low fat diet. Other factors known to affect the anticarcinogenic effects of selenium include synthetic antioxidants, vitamin E, vitamin A and ascorbic acid. The mechanisms of selenium counteraction of carcinogens remain unknown.
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