Abstract

Delayed neurotoxicity was produced in hens after the administration of a single oral dose of technical (96.43%) O-ethyl O-2,4-dichlorophenyl phenylphosphonothioate (S-Seven) in a gelatin capsule. Doses ranged from 800 to 5000 mg/kg. Hens given 5000 mg/kg also received atropine sulfate to protect them against acute toxicity. S-Seven caused loss of appetite and weight and resulted in ataxia which progressed in some hens to paralysis and death. Controls consisted of four groups of hens given a single oral dose of 500 mg/kg tri- o-cresyl phosphate (TOCP), 10 mg/kg parathion, 30 mg/kg atropine sulfate, or an empty gelatin capsule. TOCP-Treated hens developed delayed neurotoxicity while those given parathion showed weakness but subsequently recovered. Atropine sulfate and gelatin capsule controls remained normal. Degeneration of axons and myelin in the spinal cord was the most consistent histologic change and was identical to that found in TOCP control hens. Only one hen showed sciatic nerve degeneration. Three groups of hens which were given single oral doses of 100, 200, or 400 mg/kg S-Seven showed no neurologic signs of delayed neurotoxicity and their nerve tissues were not damaged. These results add strong confirmative evidence to the hypothesis that delayed neurotoxicity is a general feature of phenylphosphonothioate insecticides.

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