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Effects of ingestion of organic selenium in adapted and non-adapted rats

Published online by Cambridge University Press:  25 March 2008

W. G. Jaffe  and
Cristina Mondragon
W. G. Jaffe
Affiliation:
Instituto Nacional de Nutrición, Apartado 2049, Caracas, Venezuela
Cristina Mondragon
Affiliation:
Instituto Nacional de Nutrición, Apartado 2049, Caracas, Venezuela
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Abstract

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1. Rats were given moderate-selenium (4·5 mg/kg) or low-Se (0·5 mg/kg) diets during gestation and lactation. Their young were given diets with high (10 mg/kg), moderate or low Se contents from weaning, and groups of rats were killed at intervals during the 14-week experimental period.

2. Compared with young rats which received the low-Se diet, those which received the moderate- or high-Se diets had a high incidence of liver lesions and there were changes in liver Se content, haemoglobin concentration, packed cell volume, prothrombin activity, fibrinogen content, spleen weight, body water and serum glutamic–oxaloacetic and glutamic–pyruvic transaminase (L-aspartate: 2-oxoglutarate aminotransferase; EC 2.6.I.I and L-alanine: 2-oxoglutarate aminotransferase; EC 2.6.I.2 respectively) and alkaline phosphatase (EC 3.I.3.I) activities. In those rats which received the high-Se diet the changes were more pronounced than in those which received the moderate-Se diet.

3. In young rats from dams given moderate-Se diets, which were themselves given the moderate-Se diet, the liver Se content decreased continuously, whereas rats given the same diet but from dams which had received the low-Se diet, the liver Se content increased continuously. There was a slight improvement of symptoms of Se toxicity in all groups by the 5th week of the experimental period.

4. The results suggest that there was an adaptation to chronic Se intake.

Type
General Nutrition
Information
British Journal of Nutrition , Volume 33 , Issue 3 , May 1975 , pp. 387 - 397
Copyright
Copyright © The Nutrition Society 1975

References

Cummings, L. M., Martin, J. L. & Maag, D. D. (1965). Analyt. Chem. 37, 430.CrossRefGoogle Scholar
Hainline, A. (1958). Standard Methods of Clinical Chemistry Vol. 2, p. 49. New York: Academic Press.Google Scholar
Halverson, A. W., Palmer, I. S. & Guss, P. L. (1966). Toxic. appl. Pharmac. 9, 477.CrossRefGoogle Scholar
Jaffé W. G., Chávez, J. F. & Mondragón, M. C. (1967). Archos lat.-am. Nutr. 17, 59.Google Scholar
Jaffé W. G. & Mondragón, M. C. (1969). J. Nutr. 97, 431.Google Scholar
Jaffé W. G., Mondragón, M. C., Layrisse, M. & Ojeda, A. (1972). Archos lat.-am. Nutr. 22, 185.Google Scholar
King, E. J. & Delory, G. (1939). Biochem. J. 33, 1185.CrossRefGoogle Scholar
Natelson, S. (1961 b). Microtechniques of Clinical Chemistry 2nd ed., p. 213. Springfield, Ill.: C. C. Thomas.Google Scholar
Natelson, S. (1961 b). Microtechniques of Clinical Chemistry 2nd ed., p. 74. Springfield, Ill.: C. C. Thomas.Google Scholar
Ohmori, Y. (1937). Enzymologia 4, 217.Google Scholar
Quick, A. J. (1957). Hemorrhagic Diseases. Philadelphia: Lea & Febiger.Google Scholar
Reitman, S. & Frankel, S. (1957). Am. J. clin. Path. 28, 56.CrossRefGoogle Scholar
Rosenfeld, I. & Beath, O. A. (1964). Selenium, Geobotany, Biochemistry, Toxicity and Nutrition pp. 14, 178. New York: Academic Press.Google Scholar
Sigma Chemical Company (1963). Sigma Tech. Bull. no. 104.Google Scholar
Smith, M. I. & Lillie, R. D. (1940). Natn. Inst. Hlth Bull. no. 174.Google Scholar
US Pharmacopeia, XIV (1960). p. 789.Google Scholar