Imidacloprid activates ROS and causes mortality in honey bees (Apis mellifera) by inducing iron overload

Abstract

Imidacloprid, a neonicotinoid pesticide widely used for insect pest control, has become a potential pollutant to pollinators. Previous reports have demonstrated the toxicity of this drug in activating oxidative stress resulting in high mortality in the honey bee Apis mellifera. However, the mechanisms underlying the toxicity of imidacloprid have not been fully elucidated. In this study, sublethal (36 ng/bee) and median lethal (132 ng/bee) doses of imidacloprid were administered to bees. The results showed dose-dependent increases in reactive oxygen species (ROS), Fe2+, and mortality in bees. Notably, imidacloprid also induced upregulation of the gene encoding ferritin (AmFth), which plays a pivotal role in reducing Fe2+ overload. Upregulation of AmFth has been suggested to be closely related to ROS accumulation and high mortality in bees. To confirm the role played by AmFth in imidacloprid-activated ROS, dsAmFth double-strand was orally administered to bees after exposure to imidacloprid. The results revealed aggravated Fe2+ overload, higher ROS activation, and elevated mortality in the bees, indicating that imidacloprid activated ROS and caused mortality in the bees, probably by inducing iron overload. This study helps to elucidate the molecular mechanisms underlying the toxicity of imidacloprid from the perspective of iron metabolism.

Keywords

• Imidacloprid
• Iron metabolism
• Oxidative stress
• Apis mellifera