Selenium in Nutrition, Revised Edition (1983) / Chapter Skim
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4 BIOCHEMICAL FUNCTIONS
4 BIOCHEMICAL FUNCTIONS
Pages 40-56
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From page 40... ...
have recently reported a selenium-binding protein of unknown function in rat liver and plasma that has properties quite distinct from those of GSH-Px. In contrast to animals, microorganisms generally grow and reproduce well in the absence of selenium, a lack of certain selenium-containing enzymes being the only sign of selenium deficiency in bacteria.
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From page 41... ...
Glutathione peroxidase has been purified from the tissues of cattle, humans, swine, sheep, and rats, and shown to be an approximately 80,000dalton enzyme consisting of four apparently identical subunits (Ganther et al., 1976~. Determination of GSH-Px molecular weight by sedimentationequilibrium indicates that the molecular weight of GSH-Px differs from species to species: 76,000 + 1,000 for rat liver (Nakamura et al., 1974)
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From page 42... ...
These workers alkylated the reduced form of purified GSH-Px with iodoacetate or chloroacetate and then hydrolyzed the enzyme in hydrochloric acid. The alkylated derivatives were separated from the other amino acid residues by standard amino acid analysis procedures.
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From page 43... ...
Various lipid hydroperoxides, steroid hydroperoxides, thymine hydroperoxide, nucleic acid hydroperoxides, prostaglandin hydroperoxides, and presumably vitamin K hydroperoxide have been shown to be acceptor substrates for GSH-Px (Christophersen, 1969; Gunzler et al., 1972; Little, 1972; Nugteren and Hazelhof, 1973; Larson and Suttie, 1978~. On the other hand, cholesterol-25- and cholesterol-7ar-hydroperoxide have been reported to be poor substrates (Little, 1972)
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From page 44... ...
(1974) found that non-GSH-Px catalysis of GSH oxidation was completely eliminated by cyanomethemoglobin formation if one of the organic hydroperoxide substrates was used and the cyanomethemoglobin conversion was performed on freshly drawn blood.
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From page 45... ...
In humans, strong correlations between blood selenium and GSH-Px activity have been observed in individuals consuming low levels of selenium (Thomson et al., 1977b; McKenzie et al., 1978) , but Schmidt and Heller (1976)
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From page 46... ...
This leveling off of GSH-Px activity, but not selenium content, with increasing selenium supplementation suggests that tissue GSHPx activity may be a better indicator of effective selenium status than is tissue selenium content. Direct comparison of the biopotency of various selenium compounds for GSH-Px synthesis has shown that, in selenium-deficient chicks fed diets supplemented with less than 0.1 ppm selenium, selenite was twice as effective as selenomethionine in increasing plasma, liver, and heart GSH-Px (Noguchi et al., 1973)
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From page 47... ...
Further experiments will be necessary to establish the pathways of selenium metabolism leading to the immediate selenium precursor and the mechanism of selenium incorporation into GSH-Px. G~uTATH~oNE- S-TRANsFERAsE In 1976 it was discovered that selenium-deficient rat liver had a non-selenium-dependent GSH-Px activity (Lawrence and Burk, 1976; Prohaska and Ganther, 1976~.
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From page 48... ...
In weanling rats fed a selenium-deficient diet, liver GSH-Px activity falls to undetectable levels at about the time liver necrosis develops (Hafeman et al., 19741. In chicks, depressed plasma GSH-Px activity and the development of exudative diathesis are well correlated (Noguchi et al., 1973; Cantor et al., 1975b)
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From page 49... ...
It is unlikely that GSH-Px acts directly on fatty acid hydroperoxides in lipid membranes, but it may function by catalyzing the destruction of cytosolic hydrogen peroxide (McCay et al., 19811. A mammalian selenium-binding protein clearly different from GSH-Px was reported to be present in selenium-adequate lambs but absent in lambs suffering from nutritional muscular dystrophy (Pedersen et al., 19721.
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From page 50... ...
have noted altered metabolism of arachidonic acid via the lipoxygenase pathway in platelets from seleniumdeficient rats and have suggested that this may be the first example of a specific function for selenium as a required component in the normal metabolism of an essential fatty acid.
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, and selenium deficiency alone results in poor growth and failure to reproduce in rat pups born to selenium-deficient dams and raised on a selenium-deficient diet (McCoy and Weswig, 19691. Chicks develop muscular dystrophy, encephalomalacia, exudative diathesis, or pancreatic degeneration, depending on the presence or absence of vitamin E, selenium, sulfur amino acids, and excess dietary unsaturated fatty acids (Scott, 19781.
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From page 52... ...
Superoxide dismutase was identified as a scavenger of superoxide (McCord and Fridovich, 19691; together, superoxide dismutase and GSH-Px may prevent the reaction of superoxide with hydrogen peroxide to form hydroxy radical (Fridovich, 1975~. Ethane and pentane evolution in the breath of rats due to the peroxidative breakdown of unsaturated fatty acids also demonstrated that lipid peroxidation does occur in vivo and that such lipid peroxidation is minimized by vitamin E and dietary selenium (Dillard et al., 1977; Hafeman and Hoekstra, 1977a,b)
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From page 53... ...
The addition of sulfur amino acids to the diet delays the onset of liver necrosis in rats fed selenium- and vitamin E-deficient diets. This effect is not due solely to contamination of the sulfur amino acids by selenium (Schwarz, 1965~.
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From page 54... ...
Silver may precipitate selenide and thus make it unavailable for GSH-Px synthesis; tri-o-cresyl phosphate decreases tissue selenium levels, apparently by increasing selenium excretion. Doxorubicin, an anticancer drug that is very cardiotoxic, has been reported to reduce heart GSH-Px activity within 4 hours after injection into rabbits.
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From page 55... ...
decompose hydrogen peroxide. Unsaturated fatty acids react with oxygen to form lipid hydroperoxides.
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From page 56... ...
56 SELENIUM IN NUTRITION ther, 1980~. Reports that lead (Bell et al., 1978)
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