With the increasing demand for pollinating services, the wellness of honeybees has received widespread attention. Recent evidence indicated honeybee health might be posed a potential threat by widely used neonicotinoids worldwide. However, little is known about the molecular mechanism of these insecticides in honeybees especially at an enantiomeric level. In this study, we selected two species of bees, Apis mellifera (A. mellifera) and Apis cerana (A. cerana), to assess the toxicity and molecular mechanism of neonicotinoid dinotefuran and its enantiomers. The results showed that S-dinotefuran was more toxic than rac-dinotefuran and R-dinotefuran to honeybees by oral and contact exposures as much as 114 times. A. cerana was more susceptible to highly toxic enantiomer S-dinotefuran. S-dinotefuran induced the immune system response in A. cerana after 48 h exposure and significant changes were observed in the neuronal signaling of A. mellifera under three forms of dinotefuran exposure. Moreover, molecular docking also revealed that S-dinotefuran formed more hydrogen bonds than R-dinotefuran with nicotinic acetylcholine receptor, indicating the higher toxicity of S-dinotefuran. Data provided here show that R-dinotefuran may be a safer alternative to control pests and protect pollinators than rac-dinotefuran.
Keywords: Apis cerana; Apis mellifera; dinotefuran enantiomers; molecular mechanism; toxicity.