Imidacloprid decreases the total energy production in western honeybees even though, in sublethal doses, it increased the values of six of the nine compounds in the respiratory and citric cycle

Abstract

Neonicotinoids, including imidacloprid, harm Apis mellifera in a number of ways, among others by impairing body maintenance and immunity. Energy resources are important to prevent this, particularly, as we hypothesized, in the fat body tissue. But hormesis (adaptative, diaphasic response to a stressor) was also reported in the energy-dependent traits of bees exposed to sublethal doses of imidacloprid. Consequently, concentrations/activities of respiratory and citric cycle compounds (Acetyl-CoA, IMH-2, AKG, succinate, fumarate, NADH2, CoC, COX, and ATP) were compared in the hemolymph and fat bodies of honeybees fed with diets containing 200 ppb (IM-200), 5 ppb (IM-5; sublethal), and 0 ppb of ID. The values of the compounds were higher in the fat body than in the hemolymph, where the variability was higher in hemolymph. The pattern of response to ID was the same in both tissues, but differed between IM-200 and IM-5. The concentrations of the strongly correlated NADH2, ATP and acetyl-CoA decreased both in ID-200 and ID-5, whereas the levels of the remaining compounds decreased in ID-200 but increased in ID-5. Decreased ATP levels in each diet show that the pesticide impairs the fat-body energy metabolism in spite of hormesis in six of the nine respiratory and citric cycle compounds even in the low, residual doses. We believe that sublethal doses of imidacloprid decrease energy demands, as they decreased the levels of ATP, and acetyl-CoA.