Abstract
Selenium supplementation has been reported to suppress carcinogenesis in many different animal models. A summary of these observations can be found in several reviews.1–6 The effect is not organ specific, since selenium is known to inhibit tumor development in mammary gland, liver, skin, pancreas, esophagus, colon and other sites. In general, there is a dose dependent response, and selenium chemoprevention can be realized in the absence of toxicity. The sensitivity to selenium appears to decrease as cells progress from normal to preneoplastic to neoplastic. In order to achieve maximal prophylaxis, it is necessary to maintain a continuous regimen of selenium administration. This suggests that the active species of selenium with anticarcinogenic potential is generated only when the supply of selenium is sustained at certain levels. Metabolism alters the chemical form of selenium and plays a key role in determining its biological activity. The past collaborative work of Ip and Ganther has produced a substantial body of evidence indicating that the commonly used selenium compounds, such as selenite and selenomethionine, have to be metabolized in order to express their anticancer activity.6
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© 1996 Plenum Press, New York
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Ip, C., Lisk, D.J. (1996). The Attributes of Selenium-Enriched Garlic in Cancer Prevention. In: Dietary Phytochemicals in Cancer Prevention and Treatment. Advances in Experimental Medicine and Biology, vol 401. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0399-2_15
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DOI: https://doi.org/10.1007/978-1-4613-0399-2_15
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