Effects of excess dietary selenite on lead toxicity in sheep
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The hypothesis that excess dietary selenite ameliorates lead (Pb) toxicosis in domestic sheep was tested. Twenty 6–8-yr-old ewes fed alfalfa pellets were assigned to the following treatments: (1) control; (2) 9.8 mg Pb/kg body weight (b.w.)/d as PbCO3; (3) 3 mg Se/animal/d as Na2SeO3·5H2O; or (4) a combination of treatments 2 and 3. The gelatin-encapsulated salts were given orally. The study was terminated on d 104, by which time three animals in the Pb group and all five animals in the Pb+Se group had died. All remaining animals were slaughtered on d 104. Lead and Se concentrations were determined in six biweekly-collected blood samples and in soft tissues and bone. Sheep on the control and Se treatments had similar feed intakes, body weights, and tissue Pb levels. Those in the Pb+Se group had lower feed intake, but higher blood Pb values compared with the Pb group. Feeding either element increased (P<0.05) the concentration of that element in blood, kidney, liver, spleen, and bone. Muscle-Pb concentrations were not affected (P<0.05) by treatment. Selenium concentrations in kidney, liver, and muscle were greater (P<0.05), whereas those in heart were less (P<0.05) for the Pb+Se group than for the Se Group. Clinical signs associated with Pb toxicosis noted in other animals were not observed in the poisoned sheep in this study. Selenite did not protect sheep against Pb toxicity and likely served as a synergistic factor.
Index EntriesAlfalfa pellets blood bone kidney lead liver muscle ovine selenium sheep spleen
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- 1.National Research Council,Mineral Tolerance of Domestic Animals, National Academy of Sciences, Washington, DC, 1980, pp. 256–276, 392–420.Google Scholar
- 5.C. L. Stone and J. H. Soares,Poultry Sci. 55, 341 (1976).Google Scholar
- 6.O. E. Olson, I. S. Palmer, and E. E. Cary,J. Assoc. Off. Anal. Chem. 58, 117 (1975).Google Scholar
- 9.W. R. Harvey, US Department Agriculture, Agricultural Research Service 20–8, 1960.Google Scholar
- 10.R. G. Steel and J. H. TorriePrinciples and Procedures of Statistics, McGraw-Hill, New York, 1960, pp. 173 and 334.Google Scholar
- 11.J. J. Kaneko, inClinical Biochemistry of Domestic Animals, 3rd ed., Academic Press, New York, 1980, pp. 184–235.Google Scholar
- 12.K. R. Fick, C. B. Ammerman, S. M. Miller, C. F. Simpson, and P. E. Loggins,J. Animal Sci. 42, 515 (1976).Google Scholar
- 13.D. S. Pearl, S. B. Ammerman, P. R. Henry, and R. C. Littell,J. Animal Sci. 56, 1416 (1983).Google Scholar
- 14.K. R. Mahaffey, inLead Toxicity, R. L. Singhal and J. A. Thomas, eds., Urban and Schwarzenberg, Baltimore, 1980, pp. 425–460.Google Scholar
- 16.P. K. Ku, E. R. Miller, R. C. Wahlstrom, A. W. Groce, J. P. Hitchcock, and D. E. Ullrey,J. Animal Sci. 37, 501 (1973).Google Scholar
- 17.K. T. Mandisodza, W. G. Pond, D. J. Lisk, D. E. Hogue, L. Krook, E. E. Cary, and W. H. Gutenmann,J. Animal Sci.,49, 535 (1979).Google Scholar