tetrachlorvinphos and phosfolan

LD50 and in vitro ChE I50 values of Chlorpyrifos, Leptophos, Phosfolan, and Stirophos against white mice showed that the formulated insecticides were higher in their mammalian toxicity than the corresponding technical materials. Pretreatment of mice with a sublethal dose of Phosfolan potentiated the toxicity of post-treatment with formulated Stirophos, Phosfolan, or Chlorpyrifos, but antagonized the toxicity of post-treatment with Leptophos. On the other hand, pretreatment with sublethal doses of Leptophos resulted in potentiation of Stirophos or Phosfolan, but decreased the toxicity of Chlorpyrifos or Leptophos. Pretreatment of mice by sublethal dose of Phosfolan synergized the in vivo inhibitory power of post-treatment by Phosfolan, Chlorpyrifos or Leptophos against brain and Plasma ChE. On the other hand pretreatment with sublethal doses of Leptophos antagonized the inhibitory power of post-treatment with either Chlorpyrifos, Leptophos or Stirophos against mice brain-ChE.

Topics: Animals; Brain; Chlorpyrifos; Cholinesterase Inhibitors; Cholinesterases; Drug Synergism; Insecticides; Leptophos; Lethal Dose 50; Mice; Organothiophosphorus Compounds; Structure-Activity Relationship; Tetrachlorvinphos

Phosfolan, chlorpyrifos, and stirophos when applied to white mice at sublethal doses did not induce any delayed neurotoxic effect. On the other hand, Leptophos and EPN when administered orally at sublethal or lethal levels clearly produced a delayed neurotoxic ataxia in treated mice. The five tested organophosphorus insecticides were compared for their ability to inhibit cholinesterase, neurotoxic esterases and monoamine oxidase. I50 values were estimated for each case. The results revealed that all five compounds were inhibitors of cholinesterase, but only Leptophos and EPN were shown to be potent inhibitors for both neurotoxic esterase and monoamine oxidase in the mouse brain. Additional particular properties of both Leptophos and EPN were found in their ability to cause delayed neurotoxic ataxia in chickens and sheep fed once on sublethal doses of these compounds. It is believed that the phosphonate ester configuration of EPN and Leptophos has a specific mode of toxic action which is mainly located at the central nervous system. It is also postulated that these delayed neurotoxic agents might inhibit postganglionic sympathetic neurons, thus resulting in chronic paralytic effects.

Topics: Administration, Oral; Animals; Ataxia; Brain; Central Nervous System; Chickens; Chlorpyrifos; Cholinesterase Inhibitors; Diet; Esterases; Female; Insecticides; Leptophos; Lethal Dose 50; Mice; Monoamine Oxidase Inhibitors; Organothiophosphorus Compounds; Phenylphosphonothioic Acid, 2-Ethyl 2-(4-Nitrophenyl) Ester; Sheep; Tetrachlorvinphos