Selenium vitamin

Dietary Reference Intakes for Vitamin Q VitaminE, Selenium and Carotenoids, Food and Nutrition Board, Institutecf Medicine, National Academy Press, 2000, p. 193. 

Adapted from Food and Nutrition Board and Institute of Medicine (2000) Dietary Reference Intakes for Vitamin C, Vitamin , Selenium, and Carotenoids. Washington, DC National Academy Press. 

A large number of selenium derivatives such as the selenium analog of vitamin B] have been tested for physiological activity (91). 

Vitamin E acetate [58-95-7] serves primarily as an antioxidant and is closely associated with selenium. Vitamin E usually is present in... 

Pure selenium deficiency, without concurrent vitamin E deficiency, is not generally seen except in animals on experimental diets (113). In China, selenium deficiency in humans has been associated with Keshan disease, a cardiomyopathy seen in children and in women of child-bearing ages, and Kashin-Beck disease, an endemic osteoarthritis in adolescents (113). 

A variety of other metals and their complexes have been studied for radioprotective activity. Among these are copper glycinate, strontium chloride, ZnNa -diethylenetriaminepentaacetate (ZnDTPA), and selenium, which has been studied because of its relationship to endogenous antioxidant mechanisms, especiaHy GSH peroxidase and vitamin E. 

In 1956 selenium was identified (123) as an essential micronutrient iu nutrition. In conjunction with vitamin E, selenium is effective iu the prevention of muscular dystrophy iu animals. Sodium selenite is adrninistered to prevent exudative diathesis iu chicks, a condition iu which fluid leaks out of the tissues white muscle disease iu sheep and infertility iu ewes (see Eeed ADDITIVES). Selenium lessens the iacidence of pneumonia iu lambs and of premature, weak, and stillborn calves controls hepatosis dietetica iu pigs and decreases muscular inflammation iu horses. White muscle disease, widespread iu sheep and cattle of the selenium-deficient areas of New Zealand and the United States, is insignificant iu high selenium soil areas. The supplementation of animal feeds with selenium was approved by the U.S. EDA iu 1974 (see Eeed additives). Much of selenium s metaboHc activity results from its involvement iu the selenoproteia enzyme, glutathione peroxidase. 

There are numerous synthetic and natural compounds called antioxidants which regulate or block oxidative reactions by quenching free radicals or by preventing free-radical formation. Vitamins A, C, and E and the mineral selenium are common antioxidants occurring naturally in foods (104,105). A broad range of flavonoid or phenoHc compounds have been found to be functional antioxidants in numerous test systems (106—108). The antioxidant properties of tea flavonoids have been characterized using models of chemical and biological oxidation reactions. 

Figure 45-6. Interaction and synergism between antioxidant systems operating in the lipid phase (membranes) of the cell and the aqueous phase (cytosol). (R-,free radical PUFA-00-, peroxyl free radical of polyunsaturated fatty acid in membrane phospholipid PUFA-OOH, hydroperoxy polyunsaturated fatty acid in membrane phospholipid released as hydroperoxy free fatty acid into cytosol by the action of phospholipase Aj PUFA-OH, hydroxy polyunsaturated fatty acid TocOH, vitamin E (a-tocopherol) TocO, free radical of a-tocopherol Se, selenium GSH, reduced glutathione GS-SG, oxidized glutathione, which is returned to the reduced state after reaction with NADPH catalyzed by glutathione reductase PUFA-H, polyunsaturated fatty acid.)...

Situnayake et al., 1991). No correlation between disease activity and serum vitamin E concentrations was found, but it was su ested that such patients might suffer a reduced antioxidant capacity. However, it is conceivable that a decreased serum antioxidant status is a primary event in the evolution of RA. Recent studies (Heliovaara etal., 1994) have demonstrated that lowered levels of vitamin E, /3-carotene and selenium (required for glutathione peroxidase) together may be a risk fector for subsequent development of RA. 

Guyan et al. 1990) have used several markers of lipid peroxidation (9-cis-, 11-tmns-isomer of linoleic acid, conjugated dienes and ultraviolet fluorescent products) to demonstrate significant increases in the duodenal aspirate after secretin stimulation in patients with acute and clinic pancreatitis. They interpreted this as indicating induction of hepatic and pancreatic drug-metabolizing enzymes in the face of a shortfidl of antioxidant defences, more marked in chronic pancreatitis. Subsequent studies in patients with chronic pancreatitis have confirmed decreased serum concentrations of selenium, -carotene and vitamin E compared with healthy controls (Uden et al., 1992). Basso aol. (1990) have measured increases in lipid peroxides in the sera of patients with chronic... 

Only one study to date has been conducted on the treatment of acute pancreatitis with antioxidants. Clemens et al. (1991) were unable to show any difference in the incidence or severity of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis in a prospective, randomized, double-blind, placebo-controlled trial of allopurinol. However, Salim (1991) performed a similar trial of the effect of allopurinol and DMSO in patients with pain from recurrent pancreatitis, and found significant benefit. On the basis that depletion of antioxidants is important in the pathogenesis of chronic pancreatitis, the administration of a cocktail of antioxidants was assessed for its effect on pain in this disease. Treatment with a combination of organic selenium, d-carotene, vitamins C and E, and methionine was of benefit in the initial pilot study, and in a placebo-controlled trial (San-dilands etal., 1990 Uden et al., 1990). 

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). 

Tanner, A.R., Bantock, K.I., Hinks, L., Lloyd, B., Turner, N.R. and Wri t, R. (1986). Depressed selenium and vitamin E levels in an alcoholic population. Possible relationship to hepatic injury through increased lipid peroxidation. D. Dis. Sci. 31, 1307-1312. 

Gamsdorp, L, Gustavson, K.H., Hellstron, O. and Nordgreen, B. (1986). A trial of selenium and vitamin E in boys with muscular dystrophy. Child Neurol. 1, 211-214. 

Prevention of vascular disease is one of the goals of a study in progress in Sweden, in which newly diagnosed diabetic children have been randomized in a doubleblind study where one group receives placebo and the other a preparation containing ascorbic acid, )3-carotene, nicotinamide, selenium and vitamin E (Ludvigsson, 1992). Future research with antioxidants may attempt to prevent the onset of pancreatic beta-cell destruction in the prediabetic phase of susceptible individuals. 

Asayama, K., Kooy, N.W. and Burr, I.M. (1986). Effect of vitamin E deficiency and selenium deficiency on insulin reserve and free radical scavenging systems in islets decrease of islet manganosuperoxide dismutase. J. Lab. Clin. Med. 107, 459-463. 

Supplementation with antioxidant micronutrients, for example, vitamin E and selenium, in the elderly and in dementia subjects (Tolonen et al., 1985) has indicated that such treatments may be of some limited benefit. The value of ascorbate as a cerebroprotective antioxidant against excitotoxic neuronal injury has been proposed (Griinewald, 1993). 

Tolonen, M., Halme, M. and Sama, S. (1985). Vitamin E and selenium supplementation in geriatric patients. A doubleblind preliminary clinical trial. Biol. Trace Element Res. 7, 161-168. 

The risk of colon cancer appears to be inversely related to calcium and folate intake. Calciums protective effect may be related to a reduction in mucosal cell proliferation rates or through its binding to bile salts in the intestine, whereas dietary folate helps in maintaining normal bowel mucosa. Additional micronutrient deficiencies have been demonstrated through several studies to increase colorectal cancer risk and include selenium, vitamin C, vitamin D, vitamin E, and 3-carotene however, the benefit of dietary supplementation does not appear to be substantial.11... 

Other agents, including selenium, vitamin E, lycopene, green tea, nonsteriodal anti-inflammatory agents, isoflavones, and statins, are under investigsation for prostate cancer and show promise. Selenium is a naturally occurring trace element that is an essential nutrient in the human diet.8 However, none of these agents is currently recommended for routine use outside a clinical trial. 

Many dietary supplements have antiplatelet activity, which may increase the risk of bleeding when used concurrently with anticoagulants. Feverfew inhibits cyclooxygenase and phospholipase A2 and may interact with anticoagulants and potentiate the antiplatelet effect of aspirin. Other supplements that possess antiplatelet activity include but are not limited to garlic, ginkgo, vitamin E, vitamin A, and selenium. 

The synergistic effect observed in the presence of all three antioxidants implies that there is an interaction between the individual antioxidant components. The direct interaction of the a-tocopherol radical and ascorbic acid is already well established (Bisby and Parker 1995) and a study by Mayne and Parker (1989) on chicks deficient in vitamin E and selenium showed that the... 

In evolution parts of the code, even parts essential for independent functioning, have been lost so that higher organisms are dependent on vitamins, for example for coenzymes, and on amino acids, lipids and saccharides, or even on selenium incorporation, from other forms of life. This is selective loss in an environment of supportive organisms. Can this be random ... 

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