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Journal of Nutrition Vol. 102 No. 10 October 1972, pp. 1287-1296
Copyright © 1972 by American Society for Nutrition
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Pathology of Selenium Deficiency in the Chick1

Christian L. Gries2 and M. L. Scott

Department of Poultry Science and Graduate School of Nutrition, Cornell University, Ithaca, N. Y. 14850

Day-old chicks fed a selenium-deficient amino acid diet developed exocrine pancreatic degeneration and fibrosis, even when the diet contained added vitamin E and bile salts to maintain high plasma tocopherol levels. The time sequence study showed initial deficiency lesions at 6 days of age. These consisted of vacuolation and hyaline body formation in acinar cells and loss of zonation. Later lesions consisted of shrinkage of acinar cytoplasm toward the nuclear end of the cell, leaving an enlarging central lumen in the acinus, and the appearance of fibroblasts in the interacinar tissue. In the final stage the acinus consisted of a ring of cells composed mainly of small, dense-staining nuclei surrounding a lumen and embedded in cellular connective tissue. Necrosis of acini was seen, but rarely. Regeneration began 4 days after addition of 0.1 ppm Se to deficient diets. Acinar nuclei enlarged and became vesiculated. Cytoplasm filled the empty lumens. As acini enlarged the fibrous tissue gradually disappeared. Two weeks after selenium supplementation, the pancreas returned to a normal appearance.

KEY WORDS: • pathology • selenium • chick

1 Supported in part by U. S. Public Health Service Grant NS05632, and Hoffmann-LaRoche, Inc., Nutley, New Jersey.

2 Present address: New York State College of Veterinary Medicine, Cornell University, Ithaca, N. Y.

Manuscript received 7 October 1971.




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