On the specific molecular configuration of neurotoxic aliphatic hexacarbon compounds causing central-peripheral distal axonopathy

Peter S. Spencer, Monica C. Bischoff, Herbert H. Schaumburg

Research output: Contribution to journalArticle

104 Scopus citations

Abstract

A total of 56 young rats were fed 10 different hydrocarbon derivatives to determine the molecular configuration required for the production of nervous system disease of the type characterized by giant axonal degeneration in the distal regions of long and large, central and peripheral nerve fibers (central-peripheral distal axonopathy). For periods up to 14 weeks, animals drank ad libitum aqueous solutions containing 0.5% 2-heptanone, 0.5% 3,5-heptanedione, 0.5% 2,5-hexanedione, 0.5% 2,5-hexanediol, 0.5% 2,4-hexanedione, 0.5% 2,3-hexanedione, 0.5% 1,6-hexanediol, 0.5% 1,4-butanediol, 0.05, 0.1, or 0.25% glutaraldehyde, and 0.5 or 1% acetone. Animals treated with 2,5-hexanedione or 2,5-hexanediol failed to gain weight normally and slowly developed hindlimb weakness typical of a symmetrical peripheral neuropathy. Pathological examination of these animals revealed giant axonal swelling and secondary myelin changes in the distal regions of (1) the spino-cerebellar tracts in the cerebellar vermis and medulla oblongata, (2) the dorsal columns of the cervical, thoracic, and upper lumbar spinal cord, and (3) the sciatic, tibial, and plantar nerves. These characteristic clinical and pathological features of central-peripheral distal axonopathy failed to develop in the other groups of rats.

Original languageEnglish (US)
Pages (from-to)17-28
Number of pages12
JournalToxicology and Applied Pharmacology
Volume44
Issue number1
DOIs
StatePublished - Apr 1978

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

Fingerprint Dive into the research topics of 'On the specific molecular configuration of neurotoxic aliphatic hexacarbon compounds causing central-peripheral distal axonopathy'. Together they form a unique fingerprint.

  • Cite this