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Department of Poultry Science and Graduate School of Nutrition, Cornell University, Ithaca, New York 14850
Selenium deficiency uncomplicated by vitamin E deficiency was produced in chicks using an amino acid diet complete in all known nutrients except selenium. The development of deficiency signs was followed grossly, biochemically and histochemically. Gross signs of deficiency included growth retardation marked by particularly poor growth of muscle, liver and pancreas. These signs appeared in the chicks at 15 days of age. Early in week 4 of the experiment, pathological changes began in the pancreas. Histochemical studies showed invasion of fibroblasts and macrophages which stained strongly for acid phosphatase. At this stage, the pancreas showed a very low level of zymogen while the specific activities of the pancreatic lysosomal enzymes increased. Histochemical and biochemical studies throughout the entire experimental period showed no sign of lysosomal disruption in the acinar cells or in the invading cells, demonstrating therefore that the function of selenium in protecting the pancreas from atrophy and fibrosis does not reside in its protection of the lysosomal membranes of the pancreatic cells.
KEY WORDS: lysosomes selenium-deficiency chick pancreas acid phosphatase
1 Supported in part by U.S. Public Health Service Grant NB 05682, and by Hoffmann-LaRoche, Nutley. N. J.
2 Visiting Faculty Member, University of Tokyo, Japan.
Manuscript received 5 September 1972.