by Vincent Corbel, et al.
August 5, 2009
[Note: Cholinesterases are enzymes needed for proper functioning of the nervous system. Acetylcholinesterase is responsible for returning cholinergic neurons to resting state after activation. To read the full text of this open access article, click here.]
Background: N,N-Diethyl-3-methylbenzamide (deet) remains the gold standard for insect repellents. About 200 million people use it every year and over 8 billion doses have been applied over the past 50 years. Despite the widespread and increased interest in the use of deet in public health programs, controversies remain concerning both the identification of its target sites at the olfactory system and its mechanism of toxicity in insects, mammals and humans.
Here, we investigated the molecular target site for deet and the consequences of its interactions with carbamate insecticides on the cholinergic system.
Results: By using toxicological, biochemical and electrophysiological techniques, we show that deet is not simply a behavior-modifying chemical but that it also inhibits cholinesterase activity, in both insect and mammalian neuronal preparations. Deet is commonly used in combination with insecticides and we show that deet has the capacity to strengthen the toxicity of carbamates, a class of insecticides known to block acetylcholinesterase.
Conclusion: These findings question the safety of deet, particularly in combination with other chemicals, and they highlight the importance of a multidisciplinary approach to the development of safer insect repellents for use in public health.
Source: The open access journal BMC Biology, Aug 5, 2009. ISSN 1741-7007, by Corbel V, Stankeiwicz M, Pennetier C, Fournier D, Stojan J, Girary M, Molgo J, Hougard JM, Lapied B. Laboratoire de Lutte contre les Insectes Nuisibles, Institut de Recherche pour le Developpement, Montpellier, France. [E-mail: Vincent.corbel@ird.fr]
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