Inhibition and Recovery of Brain Cholinesterase Activity in House Flies Poisoned with Organophosphate and Carbamate Compounds1

Seventeen organophosphate, three carbamate and one sulfamate compounds were topically applied to female house flies (Musca domestica (L.)) to determine the correlation between toxicity, symptomology and in vivo inhibition of brain cholinesterase activity. The surviving flies from an LD50 dose of all the compounds went through hyperactive and paralytic symptoms and definite brain cholinesterase inhibition before recovery. Except for the carbamate, Isolan, the brain cholinesterase recovered completely with 1280 minutes and with several compounds the recovery was complete 80 minutes after treatment. The time of the highest rate of mortality in the insecticide-treated population and of paralytic symptoms in the survivors was usually closely associated with the time of maximum enzyme inhibition. Marathon was the major exception where the greatest paralysis and mortality occurred after the cholinesterase activity had shown considerable recovery. By assaying the brain cholinesterase at varying substrate concentrations it was found that at the stage of hyperactivity and early paralysis in poisoning a shift occurred in the optimum substrate concentration. This might be due to a transitory competitive stage in the cholinesterase inhibition with certain organophosphates prior to phosphorylation of the enzyme and the dephosphorylation involved in recovery. Alternative explanations are also considered.