Tellurium-Induced Demyelination

Abstract

Inclusion of elemental tellurium in the diet of young rats produces a peripheral neuropathy characterized by a highly synchronous demyelination. This is one of the few such non-immunological models available. Other models may result in an asynchronous patchwork of demyelinating and remyelinating segments (e.g., lead intoxication), or are localized to very discrete regions (e.g., demyelination induced by topical application of lysolecithin or diphtheria toxin). Morphological studies of tellurium intoxication suggest that the initial damage is to the myelinating Schwann cell (Lampert and Garrett, 1971; Hammang et al., 1986) and that vulnerability is proportional to the length of the internodal segment supported by the Schwann cell; the more myelin supported by the Schwann cell, the greater the vulnerability (Bouldin et al., 1988). It is thus uniquely suited for biochemical studies of primary demyelination. Even in the continued presence of tellurium, morphologically observable demyelination diminishes after a few days and, a week after initiation of treatment, the nerve is well launched into a phase of rapid remyelination. We are currently investigating this model with the goal of gaining a better understanding of what metabolic processes are directly affected by tellurium and, assuming there are discrete metabolic alterations, why the resultant pathology is expressed only or preferentially in myelinating Schwann cells.