VIII SIMPOSIO INTERNAZIONALE ICPBR

HAZARDS OF PESTICIDES TO BEES

Bologna, 4-6 Settembre 2002

Effetti dell’imidacloprid sulle api

Efficacy and nicotinic acetylcholine receptor binding of imidacloprid and its metabolites in Apis mellifera (Hymenoptera: Apidae): toxicological and biochemical considerations

Ralf Nauen, Ulrich Ebbinghaus-Kintscher and Richard Schmuck

Bayer AG, Bayer CropScience, Alfred-Nobel-Str. 50, D-40789 Monheim, Germany.
E-mail: richard.schmuck@bayercropscience.com

The nicotinic acetylcholine receptor (nAChR) is the molecular target of the neonicotinoid insecticide imidacloprid. Neonicotinoid insecticides are selective to insects in terms of toxicity, and this is attributed to their high agonistic affinity to insect nAChR preparations compared to those from vertebrates. Registered use patterns of imidacloprid include also soil (drench) application and seed treatment. When applied to the soil or as a seed treatment imidacloprid is metabolized more or less completely depending on plant species and time, and it has been shown that some of the metabolites appearing in planta during the degradation process are also insecticidal against aphids and whiteflies.

Here we studied the acute oral and contact toxicity of imidacloprid to adult honeybees, Apis mellifera L. var. carnica. Results indicated that both the 48-hour oral and contact LD50 of imidacloprid were in the same range, i.e. 40-100 ng/bee. Some previously reported imidacloprid metabolites occuring at low levels in planta after seed dressing, i.e. olefine-, 5-OH- and 4,5-OH-imidacloprid showed comparable or lower oral LD50-values compared to imidacloprid. The urea metabolite and 6-chloronicotinic acid (6-CNA) were not toxic at levels up to c. 100,000 ng/bee.

The pharmacological profile of the [3H]imidacloprid binding site in honeybee head membrane preparations is consistent with that anticipated for a nAChR. IC50-values for the displacement of [3H]imidacloprid by imidacloprid and several of its metabolites correlate well with the observed acute oral toxicity of the compounds in honeybees. Neurons isolated from the antennal lobe of A. mellifera and subjected to whole cell voltage clamp electrophysiology responded to the application of acetylcholine with a fast inward current, indicating the presence of nAChR´s. Imidacloprid, its olefine and 5-OH metabolite acted agonistically on these neurons, whereas all others did not induce currents at high test concentrations. The electrophysiological measurements indicated a single binding site for imidacloprid and no direct cooperativity or allosteric interaction with a second binding site.