© 1990 Oxford University Press
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Absence of Delayed Neurotoxicity and Increased Plasma Butyrylcholinesterase Activity in Triallate-Treated Hens
*Duke University Medical Center, Department of Pharmacology Durham, North Carolina 27710
Monsanto Company St. Louis, Missouri 63167
Received April 12, 1989; accepted June 29, 1989
Absence of Delayed Neurotoxicity and Increased Plasma Butyrylcholinesterase Activity in Triallate-Treated Hens. LAPADULA, D. M, JOHANNSEN, F., AND ABOU-DONIA, M. B. (1990). Fundam. Appl. Toxicol. 14, 191–198. Triallate (S-2,3,3-trichloroalryl diisopropylthiocarba-mate) was tested for the potential to produce delayed neurotoxicity. Hens were given single oral doses ranging from 312.5 to 2500 mg/kg of triallate, 750 mg/kg tri-o-cresyl phosphate (TOCP), or empty gelatin capsules on Days 1 and 21 and were killed on Day 42. In a second experiment, animals were administered daily oral doses of 25-300 mg/kg triallate or 10 mg/kg TOCP for 90 days. In a third experiment, animals were given single oral doses of 2500 mg/kg triallate, 750 mg/kg TOCP, or empty gelatin capsules and killed after 24 hr. Delayed neurotoxicity was observed only in TOCP-treated animals. Animals given daily doses of 300 mg/kg triallate became moribund after 30 days; however, histological examination revealed no lesions characteristic of organophosphorus-induced delayed neurotoxicity. Neurotoxic esterase was not significantly altered in triallate-treated animals while it was 95% inhibited in TOCP-treated animals. Plasma butyrylcholinesterase increased significantly 24 hr after treatment with triallate in a dose-dependent manner. In summary, triallate, a thiocarbamate, did not produce neurotoxicity which has been previously reported for some dithiocarbamates.