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Selenium and its Relationship to Cancer P. D. Whanger Department of Environmental and Molecular Toxicology Oregon State University Corvallis, OR 97331 The statements "Selenium may reduce the risk of certain cancers" and "Selenium may produce anticarcinogenic effects in the body" are supported by scientific evidence. There is significant scientific agreement that daily supplementation with selenium may reduce the risk of some cancers and that selenium is anticarcinogenic. This report will examine epidemiological studies, human clinical trials, animal studies, and in vitro studies on selenium's relationship to cancer. It will examine the efficacy of different forms of selenium and of different levels of selenium supplementation.
VII. Tissue cultures. The present research efforts are primarily focused on the mechanism of cancer reduction by selenium and tissue cultures have been used advantageously to study how tumors are reduced by this element. Research with these cultures also indicates that the beta-lyase mediated production of a monomethylated selenium metabolite, namely methylselenol, from SeMCYS is a key step in cancer chemoprevention by this agent (Ip et al, 2000b). In order for SeMCYS to be effective, cells must possess this beta-lyase. One way to get around this is to use methylselenic acid, which is even effective in cells without this lyase. Although several possibilities have been suggested (Combs and Gray, 1998), the evidence indicates that the likely mechanism in which selenium reduces tumors is through its effects upon apoptosis (Unni et al, 2001; Sinha et al, 1999). Methylselenic acid produced a more robust response at one-tenth the concentration of SeMCYS in the inhibition of cell proliferation and the induction of apoptosis in mouse mammary epithelial cells (Ip et al, 2000b). Apparently these cells have low levels of the beta-lyase. Interestingly the distinction between these two compounds disappears in vivo where their cancer chemopreventive efficacies were found to be very similar. The reason for this is because the beta-lyase enzyme is abundant in many tissues and thus the animal has ample capacity to convert SeMCYS to methylselenol. Work with the mouse mammary epithelial tumor cells indicate that SeMCYS mediates apoptosis by activating one or more caspases (Unni et al, 2001). Of the caspases, caspase-3 activity appeared to be activated to the greatest extent. Apparently these cells have ample lyases to convert SeMCYS to methylselenol. Further work with these same cells using methylselenic acid produced similar results, providing additional support that monomethylated forms of selenium are the critical effector molecules in selenium mediated growth inhibition in vitro (Sinha et al, 1999). Further research is needed to identify why a monomethylated form of selenium that is required for this effect cannot be fulfilled by other forms of selenium. VIII. Forms of selenium in foods and supplements. The efficacy of various selenocompounds using the mammary tumor model has been summarized in Table 1.[2][2] SeMCYS and selenobetaine are the most effective selenocompounds identified thus far against mammary tumorigenesis in animals (table 1). Although selenobetaine is just as effective, SeMCYS is considered to be the most interesting selenocompound because it is the predominant one present in selenium enriched plants such as garlic (Ip et al, 2000a), broccoli florets (Cai et al, 1995) and sprouts (Finley et al, 2001), and onions (Cai et al, 1995). Selenobetaine has never been detected in selenium enriched plants. Therefore, SeMCYS has received the most recent attention as possibly the most useful one for cancer reduction. Except for Semet and selenocystine, the other selenocompounds listed in this table are not present in plants and thus are mostly of academic interest. However, some of them are of therapeutic interest. Selenobetaine and SeMCYS are good precursors for generating monomethylated selenium (Ip, 1998). Selenobetaine tends to lose a methyl group before scission of the Se-methylene carbon bond to form methylselenol. SeMCYS is converted to methylselenol directly when cleaved by beta-lyase and unlike Semet it cannot be incorporated nonspecifically into proteins. Since these Even though Semet is effective against mammary tumors, one disadvantage is that it can be incorporated directly into general proteins instead of converted to compounds which most effectively reduce tumors (Ip, 1998). When this occurs its efficacy for tumor reduction is reduced. For example, when a low methionine diet is fed there is significant reduction in the protective effect of Semet even though the tissue selenium was actually higher in animals as compared to those given an adequate amount of methionine (Ip, 1988). When methionine is limiting, a greater percentage of Semet is incorporated nonspecifically into body proteins in place of methionine because the methionine-tRNA cannot distinguish between methionine and Semet. Feeding diets with Semet to animals as the main selenium source will result in greater tissue accumulation of selenium than other forms of selenium (Ip and Lisk, 1994; Whanger and Butler, 1989). It is not known whether this stored selenium can serve as a reserved pool of this element but the evidence indicates that it is metabolically active (Waschulewski and Sunde, 1988). With the knowledge of the effects of these selenocompounds as anticarcinogenic agents, it was of interest to investigate the most appropriate methods for delivery to the general population. One obvious approach was to investigate additional methods for expeditious ways to deliver these protective agents through the food system. One strategy in this direction was the investigation of enriching garlic with selenium (Ip et al, 1992). The addition of selenium enriched garlic to yield three micrograms selenium per gram diet significantly reduced the mammary tumor incidence in rats from 83% to 33%. Similar to garlic, selenium enriched broccoli also reduced mammary tumors from 90% to 37% (Finley et al, 2001). Selenium enriched garlic was shown to be twice as effective as selenium enriched yeast in the reduction of mammary tumors (table 2). The total number of tumors as well as the incidence of tumors was reduced to a greater extent by enriched garlic than enriched yeast. Chemical speciation of selenium in these two products indicated that Semet was the predominant form of selenium in enriched yeast whereas SeMCYS (as the glutamyl derivative) was the predominant form of selenium in enriched garlic (Ip et al, 2000a). The glutamyl derivative is considered a carrier of SeMCYS and both of these compounds were shown to be equally effective in the reduction of mammary tumors (Dong et al, 2001). These results are consistent with those in table 1 where SeMCYS was more effective than Semet for reduction of mammary tumors. The chemical composition of selenocompounds in these two sources of selenium is apparently responsible for this difference in efficacy. Using another model, selenium enriched broccoli florets (Finley et al, 2000; 2001; Finley and Davis, 2001) as well as enriched broccoli sprouts (Finley et al, 2001) significantly reduced colon tumors in rats. This is intriguing because colon cancer is the third most common newly diagnosed cancer in the United States, resulting in about 55,000 deaths per year due to this type of cancer (American Cancer Society, 2000). Selenium enriched broccoli was more effective than selenite, selenate or Semet in the reduction of induced colon carcinogenesis (Feng et al, 1999 and Davis et al, 1999). In contrast, selenite, selenate and Semet were more effective for induction of GPX activity than selenium enriched broccoli (Finley and Davis, 2001). This indicates that the plant converts the selenium to more effective forms for reduction of these tumors and these results emphasize the need to study the effects of selenium in food forms. Similar to chemically induced colon tumors there were significantly fewer intestinal tumors when mice which have a genetic defect for development of intestinal tumors were fed selenium enriched broccoli (Davis et al, 2002). These results along with data above indicate that selenium enriched broccoli is effective against both chemically and genetically induced intestinal tumors. Data from work with another strain of mice which develop spontaneous intestinal tumors is consistent with these results where selenium deficiency resulted in activation of genes involved in DNA damage (Rao et al, 2001). IX. Level of selenium necessary for nutritive benefit The Chinese data have been used almost exclusively to establish the required levels of selenium for nutritive benefit as well as to establish the safe levels for humans (Yang et al, 1989b; Yang and Zhou, 1994). It is fortunate to have a country like China where areas vary from deficient to toxic levels of selenium, and this has made it convenient to collect critical information on the metabolism and effects of various levels of selenium in humans. Significant correlations have been found between daily selenium intake and selenium content of whole blood, plasma, breast milk, and 24 hour urine (Yang et al, 1989a). Highly significant correlations were also found between levels of whole blood selenium and hair selenium, fingernail selenium and toenail selenium, hair selenium and fingernail or toenail selenium, and whole blood selenium and toenail or fingernail selenium. Morphological changes in fingernails were used as the main criterion for clinical diagnosis of selenosis (Yang et al, 1989b). The fingernail changes and loss of hair are the main signs of excess selenium intakes. With excess selenium intakes, the fingernails become brittle and are easily cracked. The data collected on Chinese subjects are summarized in table 3. An intake of nearly 5 mg of selenium resulted in definite occurrence of selenosis, characterized by hair and nail losses. One suggested reason the subjects were able to tolerate this high level of selenium is because they consumed a high fiber diet. The low adverse effect level of dietary selenium was calculated to range between 1540 and 1600 micrograms daily. However, some effects were noted in individuals with a daily intake of 900 micrograms. The maximum safe dietary selenium intake was calculated to be about 800 micrograms per day, but there were some individuals where an amount of 600 micrograms per day was the maximum safe intake. In order to provide a safety factor, the maximum safe dietary selenium intake was suggested as 400 micrograms per day. A level of about 40 micrograms daily was suggested as the minimum requirement, and an intake of less than 11 micrograms daily will definitely result in deficiency problems. Deficiency of selenium in humans results in a cardiac and muscular disorder called Keshan disease, and deficie
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[1][1] These results are consistent with some animal data. Hairless mice treated by topical application of selenomethionine (0.02%) or given drinking water with 1.5 micrograms selenium per ml as selenomethionine had significantly less skin damage due to ultraviolet irradiation (Burke et al, 1992b). This is consistent with an earlier study which indicated that dietary selenium (one microgram/g) fed to mice significantly reduced the number of skin tumors induced by two carcinogenic chemicals plus croton oil (Shamberger, 1970). [2][2] The incidence of breast cancer is greatest of all cancers in women but it is the third highest cause of all cancer deaths (American Cancer Society, 2000), probably reflecting the improved methods for detecting and treatment of breast cancer compared to other cancers . Although usually not mentioned, a small number of men develop breast cancer with even some deaths. About 400 men die of breast cancer each year compared to 43,300 breast cancer deaths in women. [3][3] The author is aware of a person who consumed one mg of selenium for two years before toxic signs of selenium occurred. Thus this element appears not as toxic as often believed.
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To Part 5 of Selenium Study
