EFFECT OF ANTICHOLINESTERASES ON ACETYLCHOLINI LEVELS IN INSECTS

Abstract

In accordance with the hypothesis for the lethal action of organophosphate insecticides, the ACh content of the nervous tissue of poisoned insects was shown to increase, and the rate of increase to depend on the degree and duration of ChE inhibition. Lethal doses of parathion, malathion, and TEPP caused increases in the ACh content of housefly heads up to 260% above normal; increased levels of ACh were also found in the thoracic nerve cord of roaches and the brains of mice after treatment with TEPP. Sublethal doses of TEPP resulted in transitory depression of ChE activity coinciding with a limited elevation of ACh levels followed by a return to normal; lethal doses resulted in prolonged inactivation of ChE and a corresponding steady increase of ACh to 90% above the normal level. Subsequent partial recovery of ChE activity, observed with lethal doses of TEPP and malathion, coincided with a fall in ACh values to below normal. At death, a portion of the ACh normally bound to tissue components is released and hydrolyzed by ChE. In contrast to the other compounds, DFP reduced the ACh levels in the heads of treated flies. The loss from the heads was associated with an equivalent gain by the rest of the body of DFP-treated flies. The ACh content of whole flies therefore remained constant (at 20% above normal) after treatment with DFP suggesting that this compound, unlike the others examined, interferes with the synthesis of ACh.