Involvement of cytoskeletal proteins in the mechanisms of organophosphorus ester-induced delayed neurotoxicity.


Journal Article (Review)

1. Organophosphorus ester-induced delayed neurotoxicity (OPIDN) is a neurodegenerative disorder characterized by the presence of swellings in the distal parts of large axons in the central and peripheral nervous systems with subsequent axonal degeneration and paralysis. 2. An early change in OPIDN is enhanced activity and autophosphorylation of Ca2+/calmodulin-dependent kinase II. 3. In OPIDN, there is also a dose- and time-dependent increase in Ca2+/calmodulin-dependent kinase mediated phosphorylation of the cytoskeletal proteins, alpha- and beta-tubulin, microtubule associated protein-2, neurofilament triplet proteins and myelin basic protein. 4. Anomalous hyperphosphorylation of neurofilaments decreases their transport rate down the axon relative to their rate of entry resulting in their accumulation. 5. Consistent with the neurochemical results is the presence of anomalous aggregations of phosphorylated neurofilaments in early stages of OPIDN. 6. These findings suggest that aberrant hyperphosphorylation of cytoskeletal proteins is a post-translational modification involved in the pathogenesis of OPIDN.

Full Text

Duke Authors

Cited Authors

  • Abou-Donia, MB

Published Date

  • May 1995

Published In

Volume / Issue

  • 22 / 5

Start / End Page

  • 358 - 359

PubMed ID

  • 7554428

Pubmed Central ID

  • 7554428

International Standard Serial Number (ISSN)

  • 0305-1870

Digital Object Identifier (DOI)

  • 10.1111/j.1440-1681.1995.tb02015.x


  • eng

Conference Location

  • Australia