Abstract
Experimental studies with rodents indicate that selenium supplementation at levels above the dietary requirement is capable of protecting against tumorigenesis induced by chemical carcinogens or viruses (1—4). With few exceptions, the selenium compounds that have been examined are those readily available from commercial sources. Over 90% of such studies reported in the literature have used either selenite or selenomethionine as the test reagent. We have compiled the results of a large number of experiments involving supplementation with either selenite or selenomethionine and compared their chemopreventive efficacies using the dimethylbenz [a] anthracene (DMBA)-induced mammary tumor model in rats. On a selenium weight basis and over a graded dose range (from 1 to 5 ppm Se in the diet), our data showed that selenomethionine was not as active as selenite in mammary cancer inhibition (5). Tissue selenium concentrations in blood, liver, kidney, and skeletal muscle, on the other hand, were always higher in rats given selenomethionine compared with those given selenite. Thus the greater total body burden of selenium in selenomethionine-treated rats did not appear to confer a better protection against tumorigenesis. Based on this observation, the question that came to mind was whether selenium metabolism is necessary for its anticarcinogenic activity.
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Ip, C., Ganther, H.E. (1994). Novel Strategies in Selenium Cancer Chemoprevention Research. In: Burk, R.F. (eds) Selenium in Biology and Human Health. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2592-8_10
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DOI: https://doi.org/10.1007/978-1-4612-2592-8_10
Publisher Name: Springer, New York, NY
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