Molecular Mechanisms of y-Diketone Neuropathy

  • Doyle G. Graham
  • Mary Beth Genter St. Clair
  • V. Amarnath
  • Douglas C. Anthony
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 283)


We know from human and animal exposure data that inhalation of high concentrations of n-hexane are required, for prolonged periods of time, before a peripheral neuropathy will develop, a product of the rates of production of its ultimate toxic metabolite and of the reactions which occur within the axon (Yamamura, 1969; Herskowitz, et al., 1971). In both human and animal species, the greater vulnerability of long over short axons is a manifestation of the greater number of molecular targets for reaction with the toxic metabolite in the longer axons and a reflection of the stability of those targets. Looking back on the 20 years that we have been aware of this neurotoxicant, it is clear that these conclusions, so important to our understanding of the molecular pathogenesis of n-hexane neuropathy, might have been drawn from the clinical observation of these patients, and, subsequently, of exposed laboratory animals.


Molecular Pathogenesis Protein Crosslinking Covalent Crosslinking Axonal Swelling Lysyl Residue 
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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Doyle G. Graham
    • 1
  • Mary Beth Genter St. Clair
    • 1
  • V. Amarnath
    • 1
  • Douglas C. Anthony
    • 1
  1. 1.Duke UniversityDurhamUSA

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