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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

Back to Part 1 of Selenium Study 

 To Part 5 of Selenium Study
ncy of selenium is thought to be one of the contributing factors to another disorder called Kaschin-Beck disease.


 

___________________________

Phil D. Whanger

Department of Environmental and Molecular Toxicology

Oregon State University

A copy of my curriculum vitae is attached

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Yasumoto, K., K. Iwami and M. Yoshida (1984) Nutritional efficiency and chemical form of selenium, an essential trace element, contained in soybean protein. Se-Te abstr. 25: 73150.

Yoshizawa K., W. C. Willett, S. J. Morris, M. J. Stampfer, D. Spiegelman, E. B. Rimm and Giovannucci. (1998) Study of prediagnostic selenium level in toenails and the risk of advanced prostate cancer. J. Natl. Cancer Inst. 90: 1219-1224

Yu, Sh.-Y., Y. J. Zhu and W. G. Li (1997) Protective role of selenium against hepatitis B virus and primary liver cancer in Qidong. Biol. Trace Elem. Res. 56: 117-124

Yu, Sh-Y. Y-J Zhu W-G Li, Q-S Huang, C. Zhi-Huang and Q-N Zhang. (1991) A preliminary report of the intervention trials of primary liver cancer in high risk populations with nutritional supple-mentation of selenium in China. Biol. Trace Elem. Res. 29: 289-294

Yu, Sh-Y., W-G Li, Y-J Zhu, W-P Yu and C. Hou (1989) Chemoprevention trial of human hepatitis with selenium supplementation in China. Biol. Trace Elem. Res. 20: 15-22

Yu, S. Y., Y. J. Chu, X. L. Gong, C. Hou, W. G. Li, H. M. Gong and J. R. Xie. (1985) Regional variation of cancer mortality incidence and its relation to selenium levels in China. Biol. Trace Elem. Res. 7: 21-29.

 

 

[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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QUESTIONS

 

 

X. Conclusion.

The RDA for selenium is 55 micrograms for healthy adults, with 40 micrograms selenium as the minimum requirement. Less than 11 micrograms selenium will definitely put people at risk of deficiency that would be expected to cause damage. Daily doses of 100 to 200 micrograms

selenium inhibit genetic damage and cancer development in humans. About 400 micrograms

selenium per day is considered an upper safe limit. Clearly doses above the RDA are needed to

inhibit genetic damage and cancer. Despite concerns about the toxicity of higher dietary levels of selenium, humans consuming up to 600 micrograms of selenium daily appear to have no adverse clinical symptoms.[3][3]

Both animal and human data indicate that more than 100 and up to 200 micrograms of selenium are necessary for greatest reduction of cancer. This is because a methylated form of selenium is necessary for maximum reduction of cancer, and the methylated forms are present at highest levels with elevated intakes of this element. In most human trials, the subjects were supplemented with 200 micrograms selenium per day and in trials where only 50 micrograms were supplemented there was not as much reduction of cancer. Therefore, the selenium requirement for maximum reduction of cancer appears to be at least four times the RDA. However, since only 50 to 200 micrograms additional selenium have been used, it is not possible to indicate which level will give maximum protection. For example, it is not known whether supplemental levels of selenium above 200 micrograms daily will provide any additional protection against cancer.

Selenium enriched yeast is the most common source of selenium available commercially and it also has been the most used selenium source in human trials. Semet is the major form in enriched yeast but SeMCYS is the predominant form in enriched plants such as garlic and broccoli. Selenium enriched garlic was shown to be twice as effective as enriched yeast in reduction of mammary tumors in rats. Apparently, the reason SeMCYS is more effective is because it is converted directly to methylselenol, the suspected biologically active form of selenium for reduction of tumors. However, it is not known whether providing twice as much selenium as enriched yeast will give the same benefits as enriched garlic. Therefore, in addition to enriched yeast, selenium enriched food plants such garlic, broccoli and onions appear also to be an effective and safe method for delivery of selenium to the general population. Nevertheless, regardless of the source of selenium it is apparent that additional intakes of this element by humans will reduce the incidence of cancer.

It has been estimated that one-third of the cancers in humans are environmentally related. The results in this report indicate that on an average there could be 50% reduction of cancer through increased selenium ingestion in humans. If the 50,000 deaths due to colorectal cancer, the 41,800 deaths due to prostate cancer in men, or the 43,300 breast cancer deaths in women could be reduced by one-half with selenium, this would be a very significant contribution to human health.

 

 

___________________________

Phil D. Whanger

Department of Environmental and Molecular Toxicology

Oregon State University

A copy of my curriculum vitae is attached

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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.