Abstract
Honey bee populations have suffered a significant decline globally in recent decades, which presents a serious danger to the ecosystem, as well as to agriculture. Food and feed production needs to rise to meet the demands of the expanding world population, which has made widespread pesticide use necessary. Neonicotinoids are widely utilized agents including acetamiprid. Given that lipids function as membrane constructing molecules, disruptions in the oxidative equilibrium within the bee's central nervous system may cause lipid peroxidation, which can change the fatty acid profile and jeopardize cell viability. Honey bees were treated with acetamiprid-containing sugar syrup for 48 hours, at concentrations of 35 µg/mL, 17.5 µg/mL and 8.75 µg/mL in the 'AcetHigh', 'AcetMedium' and 'AcetLow' groups. After dissecting the brain, the samples were homogenized, and the concentrations of the 15 most abundant fatty acids were analyzed using gas chromatography-mass spectrometry (GC-MS). The concentrations of lauric acid (C12:0), myristic acid (C14:0), palmitic acid (C16:0), stearic acid (C18:0), and alpha-linolenic acid (C18:3, n-3) were increased by acetamiprid treatment. Total fatty acid concentrations, as well as those of polyunsaturated fatty acids (PUFAs) and saturated fatty acids (SFAs), also showed elevation in acetamiprid-exposed bees, following a non-monotonic dose response. These findings imply that acetamiprid not only impacts the redox homeostasis as it was previously reported, but also adversely affects the lipid metabolism in the central nervous system of honey bees, and at the same time also triggers adaptive mechanisms.