Can Ahiflower® (Buglossoides arvensis) seed-oil supplementation help overcome the adverse effects of imidacloprid in honey bees?

In this study, we investigated the effects of nutritional supplementation as a strategy to mitigate the impacts of imidacloprid (neonicotinoid) on honey bees by using Ahiflower® (Buglossoides arvensis) seed-oil. This oil is rich in stearidonic-acid (SDA, 18:4n3), which is a precursor to eicosapentaenoic-acid (EPA) and docosahexaenoic-acid (DHA) that are known for their beneficial and protective effects. Specifically, we chronically fed newly emerged worker bees with sucrose syrup and pollen patties (control) that we supplemented with (i) imidacloprid (0.375 ng·μl⁻¹), (ii) Ahiflower® oil (5 %) + imidacloprid (0.375 ng·μl⁻¹), and (iii) Ahiflower® oil (5 %). Survival was recorded, and after 21 days, worker bees were sampled to measure mitochondrial respiration, ATP5A1 content, adenylate energy charge, lipid peroxidation in thorax as well as fatty acid composition and peroxidation index in whole bees. Our results indicate that (i) imidacloprid mostly hampers mitochondria, increases saturated fatty acids and decreases survival, (ii) oxidation of alternative substrates allows full recovery of mitochondrial respiration in the imidacloprid-treated group demonstrating mitochondrial flexibility, (iii) Ahiflower® oil in combination with imidacloprid partially restores mitochondrial respiration at the level of complexes I and II, restores fatty acid composition but fails to restore survival. These findings confirm the deleterious effects of imidacloprid on mitochondria while highlighting, for the first time, the potential benefits of Ahiflower® oil in mitochondrial function, though not on honey bee survival. In addition, this study highlights the importance of mitochondrial flexibility when organisms are exposed to toxicants at environmentally relevant levels.