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Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN).

Publication ,  Journal Article
Veronesi, B; Padilla, S; Blackmon, K; Pope, C
Published in: Toxicology and applied pharmacology
February 1991

This study reports that CD-1 strain mice are neuropathologically and biochemically responsive to acute doses of tri-ortho-cresyl phosphate (TOCP). Young (25-30 g) male and female animals were exposed (po) to a single dose of TOCP (580-3480 mg/kg) and sampled for neurotoxic esterase (NTE) activity at 24 and 44 hr postexposure and for neuropathic damage 14 days later. Biochemically, high intragroup variability existed at the lower doses, and at higher levels of TOCP exposure (i.e., greater than or equal to 1160 mg/kg), mean brain NTE inhibition never exceeded 68%. Hen and mouse brain NTE activity, assayed in vitro for sensitivity to inhibition by tolyl saligenin phosphate (TSP), the active neurotoxic metabolite of TOCP, showed similar IC50 values. Histologically, highly variable spinal cord damage was recorded throughout treatment groups and mean damage scores followed a dose-response pattern with no apparent correlation to threshold (i.e., greater than or equal to 65%) inhibition of brain NTE activity. Topographically, axonal degeneration in the mouse spinal cord predominated in the lateral and ventral columns of the upper cervical cord. Unlike the rat, which displays degeneration in the upper cervical cord's dorsal columns (i.e., gracilis fasciculus) in response to TOCP intoxication, treated mice showed minimal damage to this tract. To examine this discrepancy further, ultrastructural morphometric analysis of axon diameters in the cervical cord was performed in control mice and rats. These results indicated that in both species, the largest diameter (greater than or equal to 4 microns) axons are housed in the ventral columns of the cervical spinal cord, suggesting that axon length and diameter may not be the only criteria underlying fiber tract vulnerability in OPIDN.

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Published In

Toxicology and applied pharmacology

DOI

EISSN

1096-0333

ISSN

0041-008X

Publication Date

February 1991

Volume

107

Issue

2

Start / End Page

311 / 324

Related Subject Headings

  • Tritolyl Phosphates
  • Toxicology
  • Time Factors
  • Spinal Cord
  • Rats
  • Organophosphorus Compounds
  • Nervous System Diseases
  • Mice
  • Male
  • Female
 

Citation

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Veronesi, B., Padilla, S., Blackmon, K., & Pope, C. (1991). Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN). Toxicology and Applied Pharmacology, 107(2), 311–324. https://doi.org/10.1016/0041-008x(91)90211-v
Veronesi, B., S. Padilla, K. Blackmon, and C. Pope. “Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN).Toxicology and Applied Pharmacology 107, no. 2 (February 1991): 311–24. https://doi.org/10.1016/0041-008x(91)90211-v.
Veronesi B, Padilla S, Blackmon K, Pope C. Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN). Toxicology and applied pharmacology. 1991 Feb;107(2):311–24.
Veronesi, B., et al. “Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN).Toxicology and Applied Pharmacology, vol. 107, no. 2, Feb. 1991, pp. 311–24. Epmc, doi:10.1016/0041-008x(91)90211-v.
Veronesi B, Padilla S, Blackmon K, Pope C. Murine susceptibility to organophosphorus-induced delayed neuropathy (OPIDN). Toxicology and applied pharmacology. 1991 Feb;107(2):311–324.
Journal cover image

Published In

Toxicology and applied pharmacology

DOI

EISSN

1096-0333

ISSN

0041-008X

Publication Date

February 1991

Volume

107

Issue

2

Start / End Page

311 / 324

Related Subject Headings

  • Tritolyl Phosphates
  • Toxicology
  • Time Factors
  • Spinal Cord
  • Rats
  • Organophosphorus Compounds
  • Nervous System Diseases
  • Mice
  • Male
  • Female