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Absence of Delayed Neurotoxicity and Increased Plasma Butyrylcholinesterase Activity in Triallate-Treated Hens
Authors:LAPADULA, DANIEL M.   JOHANNSEN, FREDERICK   ABOU-DONIA, MOHAMED B.
Affiliation:*Duke University Medical Center, Department of Pharmacology Durham, North Carolina 27710 "{dagger}"Monsanto Company St. Louis, Missouri 63167

Received April 12, 1989; accepted June 29, 1989

Abstract:Absence of Delayed Neurotoxicity and Increased Plasma ButyrylcholinesteraseActivity 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 2500mg/kg of triallate, 750 mg/kg tri-o-cresyl phosphate (TOCP),or empty gelatin capsules on Days 1 and 21 and were killed onDay 42. In a second experiment, animals were administered dailyoral doses of 25-300 mg/kg triallate or 10 mg/kg TOCP for 90days. In a third experiment, animals were given single oraldoses of 2500 mg/kg triallate, 750 mg/kg TOCP, or empty gelatincapsules and killed after 24 hr. Delayed neurotoxicity was observedonly in TOCP-treated animals. Animals given daily doses of 300mg/kg triallate became moribund after 30 days; however, histologicalexamination revealed no lesions characteristic of organophosphorus-induceddelayed neurotoxicity. Neurotoxic esterase was not significantlyaltered in triallate-treated animals while it was 95% inhibitedin TOCP-treated animals. Plasma butyrylcholinesterase increasedsignificantly 24 hr after treatment with triallate in a dose-dependentmanner. In summary, triallate, a thiocarbamate, did not produceneurotoxicity which has been previously reported for some dithiocarbamates.
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