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A separation of the direct toxic effects of dietary raw egg white powder from its action in producing biotin deficiency

Published online by Cambridge University Press:  09 March 2007

J. M. Peters
Affiliation:
Department of Pharmacology, Queen's University, Kingston, Ontario, Canada
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Abstract

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1. Young adult female albino rats were given 20, 40, 60, 80, and 100% raw egg white powder in their diet; controls were fed on laboratory chow. Daily clinical measurements were made for 2 weeks. The rats were then killed, and the weights and water contents of various organs were determined.

2. The experiment was repeated with groups of young male albino rats fed for 2 and 4 weeks.

3. Toxic signs caused by increasing intake of dried raw egg white powder were: decreased food intake, weight loss, soft stool, diarrhoea, glycosuria and death. Water intake and urine output rose with increasing raw egg white powder in the diet. In all groups the urine was alkaline and the urinary output of protein increased. At autopsy there was a decrease in the absolute weight and in the water content of most body organs with increasing amounts of raw egg white powder in the diet.

4. The toxicity syndrome was not prevented by a biotin supplement, but was largely prevented by heat denaturation of the egg white powder; 80% of denatured egg white was well tolerated, as was 80% of casein in the diet.

5. The syndrome was due to the direct toxic effects of large amounts of dietary raw egg white powder and not to biotin deficiency.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1967

References

Bateman, W. G. (1916). J. biol. Chem. 26, 263.CrossRefGoogle Scholar
Bell, G. H., Davidson, J. N. & Scarborough, H. (1953). Textbook of Physiology and Biochemistry, 2nd ed. p. 101. Edinburgh: E. and S. Livingstone.Google Scholar
Boas, M. A. (1927). Biochem. J. 21, 712.CrossRefGoogle Scholar
Boyd, E. M., Peters, J. M. & Krijnen, C. J. (1966). Ind. Med. Surg. 35, 782.Google Scholar
Boyd, E. M. & Sargeant, E. J. (1962). J. New Drugs 2, 283.CrossRefGoogle Scholar
György, P. (1939). J. biol. Chem. 131, 733.CrossRefGoogle Scholar
Maignon, F. & Chahine, M. A. (1931). C. r. Séanc. Soc. Biol. 108, 868.Google Scholar
Parsons, H. T. (1931). J. biol. Chem. 90, 351.Google Scholar
Peters, J. M. & Boyd, E. M. (1966). Toxic. appl. Pharmac. 8, 350.CrossRefGoogle Scholar
Rubin, S. H., Drekter, L. & Moyer, E. H. (1945). Proc. Soc. exp. Biol. Med. 58, 352.CrossRefGoogle Scholar
Strominger, J. L. (19461947). Yale J. Biol. Med. 19, 279.Google Scholar
Tscherkes, L. A. (1927). Boichem. Z. 182, 35.Google Scholar
White, A., Handler, P. & Smith, E. L. (1964). Principles of Biochemistry, 3rd ed., p. 962. Toronto: McGraw-Hill.Google Scholar