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Cadmium Toxicity in Growing Swine1,2,

R. J. Cousins, A. K. Barber and J. R. Trout3

Department of Animal Sciences, Rutgers University, The State University of New Jersey, New Brunswick, New Jersey 08903

Cadmium (Cd) as cadmium chloride was added to the basal diet of 8-week-old swine at levels of 0, 50, 150, 450 and 1,350 ppm for a 6-week comparison period. Growth rate was decreased as a function of Cd level, having ceased in the 1,350 ppm group. Hematocrit values were the most sensitive measurement of toxicity and were decreased in all Cd-fed animals. Serum phosphorus was decreased in animals receiving 450 and 1,350 ppm Cd, while serum calcium was not affected by Cd intake. Bone ash content was decreased as a function of Cd intake. Leucine aminopeptidase (LAP) activity was depressed in renal cortex from the groups receiving 150 ppm Cd or more, but serum LAP was unaffected by Cd intake. The kidney, liver, spleen and teeth contained the highest concentrations of Cd. Kidney Cd increased with dietary Cd level but appeared to reach a near maximal level in the 450 and 1,350 ppm Cd groups. This renal Cd content was directly related to the level of cadmium-binding protein isolated from kidney cortex by gel filtration chromatography.


KEY WORDS: • cadmium • toxicity

1 Paper of the Journal Series, New Jersey Agricultural Experiment Station, New Brunswick, N. J. 08903.

2 Supported by U. S. Public Health Service Grant ES 00777-01 from the National Institute of Environmental Health Sciences: The Nutrition Foundation, Inc., Future Leader Grant No. 458: NIH BioMedical-Sciences Support Grant to Rutgers University; Rutgers University Research Council.

3 Statistical Consultant, College of Agriculture and Environmental Science, and Assistant Professor, Statistics Center, Rutgers University, The State University of New Jersey.

Manuscript received 6 December 1972.


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Hum Exp ToxicolHome page
N. G. Carmichael, B. L. Backhouse, C. Winder, and P. D. Lewis
Teratogenicity, Toxicity and Perinatal Effects of Cadmium
Human and Experimental Toxicology, March 1, 1982; 1(2): 159 - 186.
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