Abstract
Organophosphorus and carbamate insecticides are thought to have only one target site, acetylcholinesterase (EC 3.1.1.7). When this enzyme is inhibited , the neurotransmitter acetylcholine is not metabolized and polarization of the post-synaptic membrane does not take place. But, what happens when the cholinesterase becomes resistant or when neurotransmitter levels are diminished ? Here, we report results suggesting that choline acetyltransferase (EC 2.3.1.6), the enzyme responsible for the acetylcholine production, may be involved either as an alternative pesticide target site or as a factor enhancing survival during insecticide exposure. This underlines the concept that the pivotal step for insecticide toxicology is not the acetylcholinesterase activity but the amount of acetyl-choline present. This latter can only Ñuctuate between an upper and a lower threshold, and crossing one of these two thresholds leads to the death of the insect. The interaction between acetylcholinesterase and choline acetyltransferase activities would explain the astonishing toxicological phenomenon that, in some conditions, mortality decreases when insecticide concentration increases.