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Copper-deficient Diet1,2,3,
Department of Veterinary Physiology and Pharmacology, School of Veterinary Science and Medicine, Purdue University, Lafayette, Indiana
Weanling female rats of the Holtzman strain fed a copper-deficient diet (1 ppm) were mated at sexual maturity to normal males. Offspring were continued on this same diet. Within 6 weeks, some presented signs of neurologic dysfunction such as hyperirritability after noise stimulation, catatonic postures, convulsive seizures and, in male rats, priapism. Gross lesions consisted of focal pale areas in various regions of the cerebral cortex. Pathoanatomic alterations were observed in the brain with the cerebral cortex and corpus striatum consistently affected, but lesions were also present in the thalamic region of the diencephalon. Neural tissue was rarefied, spongy, edematous and obviously necrotic. Reactions to the necrosis included capillary proliferation and hemorrhage, but a significant astrocytosis was not detected. Swelling of endothelium and hyperplasia of pericytes were observed. In severely affected animals hemorrhage and liquefactive necrosis were accompanied by status spongiosus of surrounding tissue. The lesions are consistent with alterations produced by severe tissue hypoxia.
2 Supported in part by Contract no. 12-14-100-8908 (61) from the Human Nutrition Research Division ARS, USDA, Beltsville, Maryland.
3 Presented in part at the 52nd Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, New Jersey, April 1520, 1968.
Manuscript received 29 July 1968.
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