Imidacloprid disrupts larval molting regulation and nutrient energy metabolism, causing developmental delay in honey beeApis mellifera

Abstract

Imidacloprid is a global health threat that severely poisons the economically and ecologically important honeybee pollinators, Apis mellifera. However, its effects on developing bee larvae remain largely unknown. Our pilot study found that imidacloprid causes developmental delay in bee larvae, but its toxicological mechanisms are not yet fully understood. In this study, we exposed bee larvae to imidacloprid at environmentally relevant concentrations of 0.7, 1.2, 3.1, and 377 ppb. A significant dose-dependent delay in the larval development was observed, including reductions in body mass, width, and growth index; however, imidacloprid did not affect larval survival and food consumption. Predominant toxicological effects induced by high concentrations of imidacloprid (377 ppb) included disruption of neural transmission, induction of oxidative stress and gut structural damage and apoptosis, inhibition of developmental regulatory hormones and genes, disruption of proteolysis, amino acid transport, protein synthesis, carbohydrate catabolism, oxidative phosphorylation, and glycolysis energy production. In parallel, we observed that the larvae employed antioxidant defense and P450 detoxification mechanisms to counteract imidacloprid. Ultimately, this study provides the first evidence that environmental exposure to imidacloprid can retard bee larval growth and development by disrupting molting regulation and limiting the metabolism and utilization of dietary nutrients and energy. These findings have broader reference implications for studies assessing pesticide hazards to other juvenile animals.