Neuropathy target esterase in hens after sarin and soman

✍ Scribed by Crowell, J. A. ;Parker, R. M. ;Bucci, T. J. ;Dacre, J. C.

• Book ID: 102874566
• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 664 KB
• Volume: 4
• Category: Article
• ISSN: 0887-2082
• DOI: 10.1002/jbt.2570040104

✦ Synopsis

To estimate the potential of small doses of sarin (types I and 11) and soman to cause delayed neuropathic effects, 400, 200, 61, and 0 pglkg of sarin-I, 280, 140, 70, and 0 pglkg of sarin-11, and 14.2, 7.1, 3.5, and 0 pglkg of soman by gavage were compared with 510 mglkg tri-o-cresyl phosphate (TOCP) in 14to 18-month-old SPF white leghorn hens (4ldose) protected with atropine (100 mglkg). The neuropathy target esterase (NTE) adivity 24 hr after dosing was determined in brain, spinal cord, and lymphocytes and in plasma and brain for cholinesterase and carboxylesterase. None of the compounds showed statistically significant NTE decreases. Sarin-I1 showed a dose-related trend in the lymphocyte NTE (to 33% of control at 280 pglkg), suggesting that longer exposure to lower doses might cause a cumulative neurotoxic insult. All of the agents decreased the activity of plasma and brain cholinesterase and carboxylesterase. Using more than 70% inhibition of brain NTE as a biochemical predictor of delayed neuropathy, sarin and soman appear unable to cause delayed neuropathy at nonlethal doses within this protocol.