COPPER AND NERVOUS-SYSTEM - EXPERIMENTAL-STUDY
- 1 January 1977
- journal article
- research article
- Vol. 25 (5) , 299-306
Abstract
Sodium azide is known to cause changes in mammalian Cu proteins, rendering them unable to bind exogenous metal, which remains in the labile pool condition. Continuous administration of sodium azide at LD50 for 30 days causes Cu accumulation in several tissues and even in the nervous system, with characteristic changes in neurons and glial cells, very much resembling the alterations observed in Wilson''s disease. Dietary Cu administration, on the contrary, though raising the level of tissue-bound metal, does not produce cellular damage. Sodium azide may alter the Cu chelating proteins in the tissues, especially in the nervous system, causing storage of the cell-toxic labile pool metal. The pathogenesis of Wilson''s disease and pathology in the nervous system are discussed.This publication has 8 references indexed in Scilit:
- Copper deficiency and copper toxicity in the ratAmerican Journal of Physiology-Legacy Content, 1968
- Blood copper variation among speciesAmerican Journal of Physiology-Legacy Content, 1967
- Experimental striatal necrosis induced by sodium azideActa Neuropathologica, 1967
- Studies on sodium-potassium-activated adenosine triphosphataseArchives of Biochemistry and Biophysics, 1961
- IMPROVED COLORIMETRIC ENZYMATIC ASSAY OF CERULOPLASMIN1961
- A Rapid Spectrophotometric Assay of Monoamine Oxidase Based on the Rate of Disappearance of KynuramineJournal of Biological Chemistry, 1960
- STUDIES ON THE TERMINAL ELECTRON TRANSPORT SYSTEM .1. SUCCINIC DEHYDROGENASE1955
- BRAIN METABOLISM INVIVO .1. THE DISTRIBUTION OF LESIONS CAUSED BY CYANIDE POISONING, INSULIN HYPOGLYCEMIA, ASPHYXIA IN NITROGEN AND FLUOROACETATE POISONING IN RATS1950