THE PHYSIOLOGOCAL ROLE OF THE TRACE ELEMENT SELENIUM

Selenium is an element which is in traces essential for the human nutrition. Its essentiality is explained by its occurrence in various human enzymes, e.g. in four different gutathione peroxidases which act together with glutathione in the reduction of H2O2 (and prevents thus indirectly the formation of hydroxyl radicals via the Fenton reaction) and of lipid peroxides (FLOHE, 1971, HOEKSTRA, 1975; CHU, 1993). The pospholipid hydroxide glutathione peroxidase is the only enzyme capable of reduction of peroxidized fatty acids in membrane phospholipids into alcohols (KUKLINSKI, 1991). More recently Selenium was found in the I-Iodinethyronine deiodase (BEHNE, 1990; BERRY, 1991). In the plasma protein selenoprotein P (of still unknown function) seven to eight selenocysteines exist per polypeptide chain (BURK, 1991). Selenoprotein P accounts for two thirds of the Selenium present in the serum.

It is known that a too low supply of Selenium leads to an increased risk of atherosclerosis (KIEM, 1982) and cancer (SHAMBERGER, 1971; SCHRAUZER, 1977; BURNEY, 1989; HELZLSOUER, 1989). Selenium does also play a role in the detoxification of the heavy metals cadmium and mercury (PARIZEK, 1971; GASIEWICZ, 1976), in the function of the immune system (BERENSHTEIN, 1972) and probably also in the biosynthesis of cartilege (MÜLLER, 1991). Acute pancreatitis, an often lethal disease, is also caused by selenium deficiency. After administration of selenium dramatic recoveries have been observed (KUKLINSKI, 1991). SEO (2002) explains the cancer chemopreventive effect of  Selenium by a redox mechanism in which Selenomethionin activates the p53 tumor suppressor protein.

The daily requirement of selenium has been determined by LEVANDER and MORRIS (1984) by an equilibrium regression study to be 80 mcg for adult males and 57 mcg for females. The German Society for Nutrition recommends the following values as an adequate intake of selenium (DEG, 1991):

Babies mcg/day

0 to 4 months 5-15

4 to 12 months 5-30

Infants

4-7 years 15-70

7 to 10 years 15-80

above 10 years 20-100

Adults and adolsescents 20-100

A too high intake of Selenium has a toxic effect. According to COMBS (1986) the upper safe limit is 775 mcg (organically bound) selenium per adult person and day for a long term consumption. The limit for inorganic selenium is 550 mcg per person and day. According to various authors the selenium supply in many European countries is suboptimal (ROEKENS, 1986; BRÜGGEMANN, 1989). The investigation of BRUEGGEMANN (1989) showed that the daily consumption of 250 g of bread from grains harvested in Germany delivers only 10% of the minimum daily selenium requirements.

References

BEHNE, D., et al., 1990: Identification of Type I Iodothyronine 5'-Deiodinase as a Selenoenzyme. Biochem. and Biophys. Res. Comm., Vol. 173, No. 3, 1143-1149, 31.12.90

BERENSHTEIN T.F., 1972: Effect of selenium and vitamin E on antibody formation in rabbits, Zdra Wookhr. Beloruss., 18, 34 BRÜGGEMANN, J. et al., 1989: 40. Tagung für Getreidechemie in Detmold, 8.-9.6.1989

BERRY, M.J. et al., 1991: Type I iodothyronine deiodinase is a selenocysteine-containing enzyme. Nature, Vol. 349, 31 January 1991, p 438-440

BURK, R.F., 1991: Molecular biology of selenium with implications for its metabolism. FASEB Journal, vol 5, June 1991, 2274-2279

BURNEY, P.G. et al., 1989: Serologic precursors of cancer: serum micronutrients and the subsequent risk of pancreatic cancer. Am-J-Clin-Nutr. 1989 May; 49(5): 895-900

COMBS, G.F.; COMBS, St.B., 1986: The role of Selenium in Nutrition, Academic Press 1986, S. 511

CHU, F.F. et al., 1993: Expression, characterization, and tissue distribution of a new cellular Se-dependent glutathione peroxidase, GSHPx-GI. J. Biol. Chem. 1993 Feb 5; 268(4): 2571-6

DEG, 1991: Deutsche Gesellschaft für Ernährung. Empfehlungen für die Nährstoffzufuhr. S. 75

FLOHÉ, L., 1971: Die Glutathionperoxidase: Enzymologie und biologische Aspekte. Klinische Wochenschrift, 49. Jg., Heft 12, 15. Juni 1971

GASIEWICZ, T.A.; SMITH J.C., 1976: Interactions of cadmium and selenium in rat plasma in vivo and in vitro. Biochim. Biophys. Acta, 428, 113, 1976

HELZLSOUER, K.J. et al., 1989: Selenium, lycopene, alpha-tocopherol, beta-carotene, retinol, and subsequent bladder cancer. Cancer Res. 1989 Nov 1; 49(21): 6144-8

HOEKSTRA, W.G., 1975: Biochemical function of selenium and its relation to vitamin E. Federation Proceedings Vol. 34, No. 11, October 1975, 2083-2089

KIEM, J.; FEINENDEGEN, L.E., 1982: Die Beurteilung von Spurenelementen in Nahrungsketten, AGF Veranstaltung Bonn, 4.-5.11.82 KUKLINSKI, B., 1991: Akute Pankreatitis - eine "free radical desease". Letalitätssenkung durch Natriumselenit-Therapie. Z. gesamte Inn. Med. 46 (1991) 5, 145-49

LEVANDER O.E.; MORRIS, V.C., 1984: Dietary selenium levels needed to maintain balance in North American adults consuming self-selected diets. The American Journal of Clinical Nutrition 39: May 1984, pp 809-815

MÜLLER, P., 1991: Materie und Prozesse, Tagungsbericht der Deutschen Gesellschaft für Naturforscher und Ärzte, WVA, Stuttgart, S. 251 (W. Gerok ed.)

PARIZEK J. et al., 1971: The detoxifying effects of Selenium, in: Mertz, W. & Cornatzer, W.E., ed., Newer trace elements in nutrition, New York, Marcel Dekker, Inc., p. 85-122

ROEKENS E. J. et al., 1986: Dietary selenium intake in Belgium for different population groups. Z. Lebensm Unters Forsch (1986) 182:8-13 SCHRAUZER, G.N. et al., 1977: Cancer mortality correlation studies, III Statist. association with dietary Selenium intakes, Bioinorg. Chem. 7, 23. SHAMBERGER, R.J, et al., 1971: Selenium distribution of human cancer mortality, CRC Crit. Rev.: Clin Lab. Sci. 2, 211, 1971

SEO, Y. R.. et al., 2002: Selenomethionin regulation of  p53 by a ref1-dependent redox mechanism. Proc. Natl. Acad. Sci.USA, Vol 99, Issue 22, 14548-14553, October 29, 2002

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