Let op met insectenwerende middelen op basis van DEET*
Deet (N,N-diethyl-3-methylbenzamide), het actieve ingrediënt in vele insectenwerende producten, is potentieel gevaarlijk zo blijkt uit een Frans onderzoek. Bij proefdieren, insecten en muizen, werd vastgesteld dat DEET de werking van zenuwen kan verstoren en zenuwen kan beschadigen. Dit gebeurt doordat DEET het enzym acetylcholinesterase doet afremmen, zowel bij insecten als bij mensen en andere zoogdieren.
Evidence for inhibition of cholinesterases in insect and mammalian nervous systems by the insect repellent deet
Vincent Corbel1,3 , Maria Stankiewicz2 , Cédric Pennetier1,4 , Didier Fournier5 , Jure Stojan6 , Emmanuelle Girard7 , Mitko Dimitrov5 , Jordi Molgó7 , Jean-Marc Hougard3 and Bruno Lapied4
1Laboratoire de Lutte contre les Insectes Nuisibles, Institut de Recherche pour le Développement, F-34 394 Montpellier, France
2Institute of General & Molecular Biology, N. Copernicus University, 87-100 Torun, Poland
3Institut de Recherche pour le Développement/Centre de Recherches Entomologiques de Cotonou, 01 BP 4414, République du Bénin
4Laboratoire Récepteurs et Canaux Ioniques Membranaires (RCIM), UPRES EA 2647/USC INRA 2023, IFR 149 QUASAV, Université d'Angers, UFR Sciences, F-49045 Angers cedex, France
5Groupe de Biotechnologie des protéines, Université de Toulouse, Toulouse, France
6Institute of Biochemistry, Medical Faculty, University of Ljubljana, Slovenia
7CNRS, Institut de Neurobiologie Alfred Fessard – FRC2118, Laboratoire de Neurobiologie Cellulaire et Moléculaire – UPR9040, Gif sur Yvette, F-91198, France
author email corresponding author email
BMC Biology 2009, 7:47doi:10.1186/1741-7007-7-47
Abstract
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 programmes, 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 behaviour-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. (Oktober
2009)
