Title: Mechanism for the differential toxicity of neonicotinoid insecticides in the honey bee, Apis mellifera
Abstract: Laboratory bioassays were conducted to determine the contact honey bee toxicity of commercial and candidate neonicotinoid insecticides. The nitro-substituted compounds were the most toxic to the honey bee in our laboratory studies with LD50 values of 18 ng/bee for imidacloprid, 22 ng for clothianidin, 30 ng for thiamethoxam, 75 ng for dinotefuran and 138 ng for nitenpyram. The cyano-substituted neonicotinoids exhibited a much lower toxicity with LD50 values for acetamiprid and thiacloprid of 7.1 and 14.6 μg/bee, respectively. Piperonyl butoxide, triflumizole and propiconazole increased honey bee toxicity of acetamiprid 6.0-, 244- and 105-fold and thiacloprid 154-, 1,141- and 559-fold, respectively, but had a minimal effect on imidacloprid (1.70, 1.85 and 1.52-fold, respectively). The acetamiprid metabolites, N-demethyl acetamiprid, 6-chloro-3-pyridylmethanol and 6-chloro-nicotinic acid when applied topically, produced no mortality at 50 μg/bee. These results suggest that P450s are an important mechanism for acetamiprid and thiacloprid detoxification and their low toxicity to honey bees. When honey bees were placed in cages in forced contact with alfalfa treated with acetamiprid and the synergist, triflumizole, in combination at their maximum recommended application rates, no mortality was detected above that of the control.
Publication Year: 2003
Publication Date: 2003-10-31
Language: en
Type: article
Indexed In: ['crossref']
Access and Citation
Cited By Count: 677
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot