Pathogenetic studies of hexane and carbon disulfide neurotoxicity.

Graham DG, Amarnath V, Valentine WM, Pyle SJ, Anthony DC
Crit Rev Toxicol. 1995 25 (2): 91-112

PMID: 7612176 · DOI:10.3109/10408449509021609

Two commonly employed solvents, n-hexane and carbon disulfide (CS2), although chemically dissimilar, result in identical neurofilament-filled swellings of the distal axon in both the central and peripheral nervous systems. Whereas CS2 is itself a neurotoxicant, hexane requires metabolism to the gamma-diketone, 2,5-hexanedione (HD). Both HD and CS2 react with protein amino functions to yield initial adducts (pyrrolyl or dithiocarbamate derivatives, respectively), which then undergo oxidation or decomposition to an electrophile (oxidized pyrrole ring or isothiocyanate), that then reacts with protein nucleophiles to result in protein cross-linking. It is postulated that progressive cross-linking of the stable neurofilament during its anterograde transport in the longest axons ultimately results in the accumulation of neurofilaments within axonal swellings. Reaction with additional targets appears to be responsible for the degeneration of the axon distal to the swellings.

MeSH Terms (6)

Animals Carbon Disulfide Hexanes Humans Illicit Drugs Nervous System Diseases

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