Insecticide poisoning organophosphate compounds

C. Bronchoconstriction and secretion and muscular weaknesses occur from acetylcholine accumulation after inhibition of acetylcholinesterase. Parathion is an organophosphate insecticide that inhibits acetylcholinesterase, and it is readily available. Poisoning with compound 1080 (fluorocitrate) inhibits mitochondrial respiration and causes seizures and car-... 

Still another experimental route to introducing otherwise excluded molecules into the brain is to chemically modify them so that they are lipophilic and therefore can passively diffuse. The brain, just as most other organs and tissues of the body, has enzymes to metabolize or biotransform metabolites in order to use and then get rid of them. Many of these pathways are oxidative. A reduced species or derivative which is lipophilic can enter the brain by simple passive diffusion there to be oxidatively transformed into an active state. Compounds which have been tested in animals include derivatives of 2-PAM (an antidote for organophosphate insecticide poisoning) and phenylethylamine (similar to amphetamine type molecules). Figure 5 illustrates the general concept behind this method. 

In summary, studies intended to examine the neuropsychiatric effects of organophosphate compounds vary in their adequacy, and in some instances the results are contradictory. Most studies agree, however, that acute neuropsychiatric effects result from exposure to both insecticides and nerve agents. These effects include inability to concentrate, memory problems, sleep disturbances, anxiety, irritability, depression, and problems with information processing and psychomotor tasks. With pesticides, these effects do not occur in the absence of the conventional signs of poisoning. 

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