Mitochondrial Dysfunction: A Plausible Pathway for Honeybee Colony Collapse Disorder (CCD)

摘要

Neonicotinoids, the most widely used systemic insecticides in the world, have been shown to be one of the risk factors to colony collapse disorder (CCD). Although the exact underlying mechanisms of honeybee (Apis mellifera) CCD have not yet been confirmed, we postulated that mitochondrial DNA ( mtDNA) damage in honeybees resulting from sublethal neonicointoids exposure could be a plausible cause leading to malfunctioning thermoregulation. In this study, we used the relative mitochondrial DNA copy number (RmtDNAcn) as an early biomarker to elucidate the association between chronic sublethal neonicotinoids exposure and mtDNA damage in honeybees. We collected adult worker bees from hives that were either served as controls or exposed to a sub-lethal level of imidacloprid or clothianidin in three different brood generations that coincided with before, during, and after neonicotinoids treatments. Although there were no apparent adverse health effects in individual bees or the whole colony during and after neonicotinoids administration, the cumulative mtDNA damage in winter bees might have negatively impacted their hives' survival over winter due to the perturbation of energy metabolism. These results contribute to the explanation of a potential mechanism of CCD.