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Selenium dietary

Selenocysteine was identified in 1976 (57) in a protein produced by Clostridium stricklandii, and it is thought to be the form in which selenium is incorporated, stoichiometricaHy, into proteins. Studies with rats show that over 80% of the dietary selenium given them is incorporated into proteins, thus selenocysteine takes on metaboHc importance. Selenoproteins having known enzymatic activities contain selenocysteine at the active sites. Two other forms of metabohc selenium are recognized methylated selenium compounds are synthesized for excretion, and selenium is incorporated into some transfer ribonucleic acids (tRNAs) in cultured cells (58). Some of the more important seleno-compounds are Hsted in Table 4. Examples of simple ring compounds are shown in Eigure 4. [Pg.333]

Combs, G.F. and F.J. Peterson. 1983. Protection against acute paraquat toxicity by dietary selenium in the chick. Jour. Nutr. 13 538-545. [Pg.1187]

Cleveland, L., E.E. Little, D.R. Buckler, and R.H. Wiedmeyer. 1993. Toxicity and bioaccumulation of waterborne and dietary selenium in juvenile bluegill (Lepomis macrochirus). Aquat. Toxicol. 27 265-280. [Pg.1624]

Coyle, J.J., D.R. Buckler, C.G. Ingersoll, J.F. Fairchild, and T.W. May. 1993. Effect of dietary selenium on the reproductive success of bluegills (Lepomis macrochirus). Environ Toxicol. Chem. 12 551-565. [Pg.1624]

Beije, B., Onfelt, A. Olsson, U. (1984) Influence of dietary selenium on the mutagenic activity of perfusate and bile from rat liver, perfused with 1,1-dimethylhydrazine. Mutat. Res., 130, 121-126... [Pg.1433]

In terms of human dietary requirements, much of the wheat for breadmaking in the United States is produced in selenium-adequate sections of the country. Bread is generally a good source of dietary selenium, Selenomethionine decomposes lipid peroxides and inhibits in vivo lipid peroxidation in tissues of vitamin-E-deficient chicks. Selenocysdne catalyzes the decomposition of organic hydroperoxides. Selenoproteins show a high degree of inhibition of lipid peroxidation in livers of sheep, chickens, and rats, Thus, some forms of selenium exhibit in vivo antioxidant behavior,... [Pg.1465]

Kenyon, E.M., Hughes, M.F. and Levander, O.A. (1997) Influence of dietary selenium on the disposition of arsenate in the female B6C3F1 mouse. Journal of Toxicology and Environmental Health-Part A, 51(3), 279-99. [Pg.269]

Excess dietary selenium has to be avoided because of its potential toxicity at high levels in the diet and the various feed regulations are designed to prevent this occurrence. [Pg.41]

In growing chicks, a deficiency can result in (i) encephalomalacia or crazy chick disease (ii) exudative diathesis, an oedema caused by excessive capillary permeability or (iii) muscular dystrophy. Encephalomalacia occurs when the diet contains unsaturated fats that are susceptible to rancidity. Some antioxidants, in addition to vitamin E, are also effective against encephalomalacia. Exudative diathesis is prevented by dietary selenium, and muscular dystrophy is a complex disease influenced by vitamin E, selenium, and the... [Pg.45]

In five of six nondietary tumor-promotion experiments, sodium selenide significantly reduced the number of mice with tumors induced by 7,12-dimethyl-benzanthracene (DMBA)-croton oil (1). In these experiments, sodium selenide was applied concomitantly along with croton oil to female Swiss albino mice initiated with DMBA. Riley has also observed a reduction in DMBA-phorbol ester carcinogenesis by sodium selenide (2). The effect of selenium-deficient and selenium-adequate diets on DMBA-croton oil and benzopyrene skin carcinogenesis has also been studied. Supplemental dietary selenium inhibited both types of carcinogenesis. [Pg.118]

Two types of epidemiological relationships have been found in two different populations. Both relationships were inverse to selenium bioavailability and paralleled the results from animal studies. In one type of study, selenium bioavailability has been inversely related to human cancer mortality in American cities and states (14-15). Schrauzer et.al. correlated the age-adjusted mortality from cancer at 17 major body sites with the apparent dietary selenium intakes estimated from food consumption data in 27 countries (16). Significant inverse correlations were observed for cancers of the large intestine, rectum, prostate, breast, ovary, lung, and leukemia. In addition, weaker inverse associations were found for cancers of the pancreas, skin, and bladder. [Pg.119]

Selenium has been reported to have a positive, enhancing effect (42) or an inverse correlation between the intake of selenium and colon cancer (43,44). Birt et al (45) have reported inhibition of colon cancer in rats by dietary selenium. [Pg.173]

Numerous scientists have also demonstrated that dietary selenium supplementation can inhibit chemical carcinogen induced tumorigenesis in skin, liver, colon and mammary tissue (19-45)... [Pg.268]

Table II. Effect of Dietary Selenium on the Incidence of Mammary Tumors in C H/St Mice... Table II. Effect of Dietary Selenium on the Incidence of Mammary Tumors in C H/St Mice...
Sayar, K., Ugur, M., Gurdal, H., Onaran, O., Hotomaroglu, O., and Turan, B. 2000. Dietary selenium and vitamin E intakes alter p-adrenergic response of L-type Ca-current and P-adrenoceptor-adenylate cyclase coupling in rat heart. J. Nutr. 130 733-740. [Pg.48]

Fig. 8.3 Effects of dietary selenium on p-adrenergic responses in rat heart, (a) L-type Ca2+ currents (I(a i recorded from ventricular myocytes with depolarization from —70mV to OmV, for 200 ms. Mean ( SEM) values of peak amplitudes of IcaL in both experimental and control groups. The cell capacitances of these three groups of cardiomyocytes were similar, (b) Average current-voltage relationships for peak IcaL (measured as the difference between the peak Ca2+ current and the end of 200-ms depolarization). The maximums of IcaL of both experimental groups were shifted to the right with respect to the control, (c) The threshold potentials were significantly more negative and activation potentials were more positive in both experimental groups with respect to the control. (Adapted from Sayar et al. 2000.)... Fig. 8.3 Effects of dietary selenium on p-adrenergic responses in rat heart, (a) L-type Ca2+ currents (I(a i recorded from ventricular myocytes with depolarization from —70mV to OmV, for 200 ms. Mean ( SEM) values of peak amplitudes of IcaL in both experimental and control groups. The cell capacitances of these three groups of cardiomyocytes were similar, (b) Average current-voltage relationships for peak IcaL (measured as the difference between the peak Ca2+ current and the end of 200-ms depolarization). The maximums of IcaL of both experimental groups were shifted to the right with respect to the control, (c) The threshold potentials were significantly more negative and activation potentials were more positive in both experimental groups with respect to the control. (Adapted from Sayar et al. 2000.)...
Jacques, K.A. 2001. Selenium metabolism in animals the relationship between dietary selenium form and physiological response. In Science and Technology in the Feed Industry (T.P. Lyons and... [Pg.106]

McAdam, P.A. and Levander, O.A. 1987. Chronic toxicity of dietary selenium fed to rats as D- or L-selenomethionine, selenite or selenate. Nutr. Res. 7, 601-610. [Pg.107]


See other pages where Selenium dietary is mentioned: [Pg.78]    [Pg.698]    [Pg.937]    [Pg.1615]    [Pg.1616]    [Pg.1616]    [Pg.937]    [Pg.1661]    [Pg.1662]    [Pg.1662]    [Pg.118]    [Pg.118]    [Pg.268]    [Pg.270]    [Pg.271]    [Pg.272]    [Pg.276]    [Pg.277]    [Pg.163]    [Pg.164]    [Pg.269]    [Pg.104]   
See also in sourсe #XX -- [ Pg.342 ]




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Selenium Requirements and Recommended Dietary Intakes

Selenium dietary sources

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