COPPER AND NERVOUS-SYSTEM - EXPERIMENTAL-STUDY

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.