Sessions

The increasing decline in honeybees and numerous wild pollinator species can be attributed, among other factors, to the harmful effects of pesticides used in crop protection. In our study, deltamethrin, a pyrethroid widely used in agriculture, was selected for investigation. It is known that this active ingredient causes paralysis and death at lethal doses, and that even after mild exposure, cognitive and motor dysfunction develops in insects, including honeybees, which are not considered target organisms. However, the neurochemical mechanisms underlying the changes induced by sublethal exposure are not yet fully understood. Therefore, it was investigated whether sublethal oral exposure to deltamethrin causes changes in fatty acid homeostasis in the honeybee brain.

During the study, forager bees were treated with deltamethrin at three field-realistic concentrations (oral LD50/40, LD50/20, and LD50/10) for 48 hours. The bees’ brains were then dissected, and the fatty acid composition was determined using gas chromatography–mass spectrometry (GC-MS). For each group, ten composite samples were prepared (two per treatment unit), each containing a pooled sample from the brains of four bees. During the measurement, changes in the concentrations of the 15 most abundant fatty acids in the bees’ fatty acid profile were specifically examined, and changes in the amounts of saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids were also monitored. As a result of the treatment, a marked, dose-dependent increase was observed in the total fatty acid content, as well as in the levels of SFAs, MUFAs, and PUFAs. In addition, particularly following exposure to medium and high doses, the levels of stearic acid, oleic acid, linoleic acid, and linolenic acid, among others, increased significantly compared to the control group. All of this highlights that deltamethrin can induce fatty acid accumulation in the brain by disrupting lipid metabolism. Consistent with this, it was demonstrated in a previous study of our research group that deltamethrin also disrupts redox processes in bees. Oxidative stress and fatty acid accumulation together can create a lipotoxic environment, which may lead to reduced membrane integrity and impaired synaptic function.

Overall, our results present the disruption of fatty acid homeostasis as a possible mechanism of deltamethrin neurotoxicity and support the inclusion of sublethal biochemical markers in pesticide risk assessments to protect pollinators. Our observations are therefore relevant to both basic and applied research.