Tellurium-induced neuropathy: metabolic alterations associated with demyelination and remyelination in rat sciatic nerve.

作者: G. J. Harry , J. F. Goodrum , T. W. Bouldin , M. Wagner-Recio , A. D. Toews

DOI: 10.1111/J.1471-4159.1989.TB02545.X

关键词:

摘要: Rats fed a diet containing 1.25% elemental tellurium initiated on postnatal day 20 undergo transient neuropathy characterized by synchronous demyelination of peripheral nerves. In sciatic nerve, the extent was maximal after 5 days exposure; there loss 25% myelin, as assayed concentration myelin-specific P0 protein. Tellurium-induced alterations in metabolic capacity Schwann cells were examined measuring synthesis myelin lipids vitro isolated nerve segments. Exposure to resulted an early marked decrease approximately 50% overall incorporation [14C]acetate into lipids, with preferential depression cerebrosides, cholesterol, and ethanolamine plasmalogens (components enriched myelin). Most dramatically, within 1 initiation exposure, profound increase [14C]acetate-derived radioactivity squalene; 23% incorporated label this intermediate cholesterol biosynthesis, compared less than 0.5% controls. association remyelinating phase seen components gradually returned normal levels. After 30 days, morphologic no longer apparent. We suggest that sequence events following treatment initially involves inhibition conversion squalene 2,3-epoxysqualene, block biosynthesis pathway results, either directly or indirectly, breakdown myelin.

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