The statements "Selenium may reduce the risk of certain cancers" and "Selenium may produce anticarcinogenic effects in the body" are supported by scientific evidence


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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.

III. Selenocompounds in animals

A brief metabolic pathway for selenium metabolism in animals has been presented (Ip, 1998). Organic selenium such as Semet or inorganic selenium can be converted to a common intermediate, hydrogen selenide. There are two possible pathways for the catabolism of Semet. One is the transsulfuration pathway via selenocystathionine to produce selenocysteine, which in turn is degraded to hydrogen selenide by the enzyme, $-lyase (Mitchell and Benevenga, 1978). The other pathway is the transamination-decarboxylation pathway. It was estimated that 90% of the methionine is metabolized through this pathway and thus could be the major route also for Semet catabolism. SeMCYS is the predominant selenocompound formed in selenium enriched garlic at relatively low concentrations, but g-glutamyl-Se methyl selenocystine is the predominant one at high selenium concentrations (Dong et al, 2001). Even though this glutamyl derivative may be the predominant one, it is hydrolyzed in the intestinal tract and the absorbed SeMCYS cleaved by a lyase to form methylselenol (Dong et al, 2001). Thus, this glutamyl derivative is metabolized like SeMCYS at the tissue level. SeMCYS is converted to methylselenol directly when cleaved by beta-lyase and unlike Semet it cannot be incorporated nonspecifically into proteins. Since SeMCYS can be converted directly to methylselenol, this is presumably the reason it is more efficacious than other forms of selenium.

When rats are injected with selenite, the majority of the selenium is present in tissues as selenocysteine (Olson and Palmer, 1976; Beilstein and Whanger, 1988). As expected, no Semet was found under the conditions of these studies. In contrast to plants, there is no known pathway in animals for synthesis of Semet from inorganic selenium, and thus they must depend upon plant or microbial sources for this selenoamino acid. However, animals can convert Semet to selenocysteine. One day after injection of Semet there is about three times as much Semet as selenocysteine in tissues, but five or more days afterwards the majority (46-57%) of the selenium is present as selenocysteine (Beilstein and Whanger, 1986).

A total of 24 selenoproteins have been identified in eukaryotes (Gladyshev, 2001). These selenoproteins have been subdivided into groups based on the location of selenocysteine in selenoprotein polypeptides. The first group (called glutathione peroxidase, GPX) is the most abundant and includes proteins in which selenocysteine is located in the N-terminal portion of a relatively short functional domain. These include the four GPXs, selenoproteins P, Pb, W, W2, T T2 and BthD (from Drosophila). The second group of eukaryotic selenoproteins is characterized by the presence of selenocysteine in C-terminal sequences. These include the three thioredoxin reductases and the G-rich protein from Drosophila. Other eukaryotic selenoproteins are currently placed in the third group that consists of the three deiodinase isozymes, selenoproteins R and N, the 15 kDa selenoprotein and selenophosphate synthetase. The four GPXs are located in different parts of tissues and all detoxify to various degrees hydrogen peroxide and fatty acid derived hydroperoxides and thus are considered antioxidant selenoenzymes. The three deiodinases convert thyroxine to triiodothyronine, thus regulating thyroid hormone metabolism. The thioredoxin reductases reduce intramolecular disulfide bonds and, among other reactions, regenerate vitamin C from its oxidized state. These reductases can also affect the redox regulation of a variety of factors, including ribonucleotide reductase, the glucocorticoid receptor and the transcription factors (Holmgren, 2001). Selenophosphate synthetase synthesizes selenophosphate, which is a precursor for the synthesis of selenocysteine.(Mansell and Berry, 2001). The functions of the other selenoproteins have not been definitely identified.

Selenium is present in all eukaryotic selenoproteins as selenocysteine (Gladyshev, 2001). Semet is incorporated randomly in animal proteins in place of methionine. By contrast, the incorporation of selenocysteine into proteins known as selenoproteins is not random. Thus, by contrast to Semet, selenocysteine does not randomly substitute for cysteine. In fact, selenocysteine has it own triplet code (UGA) and is considered to be the 21st genetically coded amino acid. Interestingly, UGA has a dual role in the genetic code, serving as a signal for termination and also a codon for selenocysteine. Whether it serves as a stop codon or encodes selenocysteine depends upon the location of what is called the selenocysteine insertion sequence (Mansell and Berry, 2001).

A number of reviews have been written on the chemopreventive effects of selenium including most recently those by Combs and Gray (1998), Ganther (1999), Ip (1998), Schrauzer (2000), El-Bayoumy (2001) and Fleming et al (2001). The mechanism for selenium as an anticarcinogenic element is not known but several speculations have been advanced. It is well established that the most effective dose of selenium for cancer protection is at elevated levels, often called supernutritional or pharmacological levels. The suggested mechanisms for cancer prevention by selenium include its effects upon cell cycle (called apoptosis, probably the most accepted possibility), its role in selenoenzymes, its effects upon carcinogen metabolism, its effects upon the immune system, and its specific inhibition of tumor cell growth by certain selenium metabolites.



IV. Epidemiological studies.

There have been a number of epidemiological studies in the United States and throughout the world on the relationship between selenium and cancer. Shamberger and Frost (1969) reported that the selenium status of humans may be inversely related to the risk of some kinds of cancer. Two years later, Shamberger and Willis (1971) in more extensive studies indicated that the mortality due to lymphomas and cancers of the gastrointestinal tract, peritoneum, lung, and breast were lower for men and women residing in areas of the United States that have high concentrations of selenium in forage crops than those residing in areas with low selenium content in the forages. Those studies were supported by a later analysis of colorectal cancer mortality using the same forage data (Clark et al, 1981). A 27-country comparison revealed that total cancer mortality rate and age-corrected mortality due to leukemia and cancers of the colon, rectum, breast, ovary and lung varied inversely with estimated per capita selenium intake (Schrauzer et al, 1977). Similar results were also reported in China, a country where selenium intakes range from deficient to toxic levels (Yu et al, 1985).

Lower selenium levels were found in serum collected from American subjects one to five years prior to diagnosis of cancer as compared to those who remained cancer free during this time (Willett et al, 1983). That association was strongest for gastrointestinal and prostatic cancers. Evidence that low serum selenium is a prediagnostic indicator of higher cancer risk was subsequently shown in studies conducted in Finland (Salonen et al, 1984) and Japan (Ujiie et al, 1998). In additional case-control studies, low serum or plasma selenium were found to be associated with increased risk of thyroid cancer (Glattre et al, 1989), malignant oral cavity lesions (Toma et al, 1991), prostate cancer (Brooks et al, 2001), esophageal and gastric cancers (Mark et al, 2000), cervical cancer mortality rates (Guo et al, 1994) and colorectal adenomas (Russo et al, 1997). A decade long prospective study of selenium status and cancer incidences indicated that initial plasma selenium concentration was inversely related to subsequent risks of both non-melanoma skin cancer and colonic adenomatous polyps (Clark et al, 1993). Patients with plasma selenium levels less than 128 ng/ml (the average normal value) were four times more likely to have one or more adenomatous polyps. An 8-year retrospective case control study in Maryland revealed no significant association of serum selenium level and cancer risk at sites other than the bladder (Helzlsouer et al, 1989), but those with low plasma selenium levels had a 2-fold greater risk of bladder cancer than those with high plasma selenium. In a study with Dutch patients the mean selenium levels were significantly less than that of controls in men, but no differences were found in plasma selenium levels between control women and those with cancer (Kok et al, 1987). No significant associations in three other studies were found between serum selenium concentration and risk to total cancers (Coates et al, 1988) or cancers of the lungs, stomach, or rectum (Nomura et al, 1987 and Kabuto et al, 1994). In other work, significant increases of urinary selenium excretion were found in Mexican women with cervical uterine cancer as compared to controls (Navarrete et al, 2001).

In four studies low toenail selenium values were associated with higher risks of developing cancers of the lung (van den Brandt et al, 1993a), stomach (van den Brandt et al, 1993b), breast (Garland et al, 1995) and prostate (Yoshizawa et al, 1998). In contrast, in four other studies no significant differences were found between cancer cases and controls (Noord et al, 1987, Hunter et al, 1990, Rogers et al, 1991 and Veer et al, 1990). It has been suggested that the reason for those not showing a relationship is because the selenium intakes of most of the subjects tested were below that necessary for protection (Schrauzer, 2000). Obviously these results indicate that many factors must be taken into consideration when evaluating plasma and toenail selenium concentrations in relation to cancer incidence.

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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.

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