DELAYED NEUROTOXICITY OF SUB-CHRONIC ORAL-ADMINISTRATION OF LEPTOPHOS TO HENS - RECOVERY DURING 4 MONTHS AFTER EXPOSURE

Daily orai administration of small doses of technical grade O-methyl 0-4-bromo-2,5- dichiorophenyi phenyiphosphonothioate (leptophos, 0.5-20.0 mg/kg) caused delayed neurotoxicity in hens. Severity of clinica! condition and progression or improvement of signs of delayed neurotoxicity depended on the dose and duration of administration. Hens given 20.0 mg/kg suffered ataxia, paralysis, and death. Intermediate doses (5 and 10 mg/kg) caused ataxia, with most treated hens showing no change in clinical condition during the 4-mo observation period. Hens given small doses (2.5 and 1.0 mg/kg) demonstrated regression of neurological deficits after administration of leptophos was stopped. Hens given the smallest tested dose (0.5 mg/kg) developed mild ataxia and showed total recovery during the observation period. Days of administration and total administered dose before onset of ataxia depended on the daily dose. Degeneration of axons and myelin in the spinai cord was the most consistent histopathologic change and was identical to that observed in tri-o-cresyl phosphate (TOCP) control hens. Only one hen, which died early in the treatment period, showed peripheral nerve degeneration. Controls consisted of 3 groups of hens given a daily orai dose of 10.0 mg/kg TOCP, 1.0 mg/kg 0,0-diethyl O-4-nitrophenyl phosphorothioate (parathion), or an empty gelatin capsule. TOCP-treated hens developed delayed neurotoxicity, whereas those given parathion showed initiai leg weakness but subsequently recovery without developing delayed neurotoxicity. Controls given gelatin capsules remained normal. © 1979 Taylor & Francis Group, LLC.