Titlebook: Insecticide Action; From Molecule to Org Toshio Narahashi,Janice E. Chambers Book 1989 Plenum Press, New York 1989 GABA.Glutamat.Mammalia.N

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Studies on the Molecular Pathogenesis of Organophosphorus Compound-Induced Delayed Neurotoxicity (Or a delay period of 6 to 14 days, neurologic dysfunctions are manifested as ataxia and bilateral paralysis. Early lesions are aggregates of neurotubules and neurofilaments which later condense. Neurotoxic doses of TOCP resulted in an increased activity of Ca.-calmodulin kinase II (CaM kinase II). Th

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Physiological Compensation for Toxic Actions of Organophosphate Insecticides,nophosphate anticholinesterase were studied concurrently with behavioral deficits resulting from the intoxication. Paraoxon, the active metabolite of the common insecticide parathion, was administered to male rats at lethal (antidoted with atropine) and high sub-lethal levels. Brain acetylcholineste

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Monooxygenations: Interactions and Expression of Toxicity,. Toxicity in vivo, however, is considerably modulated by rates of absorption, metabolism, and elimination of the insecticide; thus, metabolic fate plays a pivotal role in the toxicity and persistence of insecticides. Species variance in toxicity is often due to differential rates or routes of biotr

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Non-Catalytic Detoxication of Acetylcholinesterase Inhibitors by Liver and Plasma Proteins,d in catalytic degradation have received the greatest attention. Some years ago, however, it was proposed that interaction of toxicants with non-target sites could serve to reduce the potential toxicity of the chemical. This process would be particularly effective with irreversible enzyme inhibitors

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