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Honey bees together with wild pollinators are increasingly threatened by environmental contaminants, including widely used pyrethroid insecticides. While sublethal exposure to deltamethrin is known to impair honey bee cognition and foraging behavior, the underlying neurochemical mechanisms remain incompletely understood. In this study, we investigated whether acute oral exposure to sublethal doses of deltamethrin disrupts fatty acid homeostasis in the honey bee brain. Forager workers were exposed for 48 h to three field-realistic concentrations of deltamethrin corresponding to daily LD50/40, LD50/20 and LD50/10, while controls received solvent-matched sucrose solution. Brain fatty acid composition was quantified by gas chromatography-mass spectrometry, and multivariate analyses were applied to characterize treatment-related metabolic shifts. Deltamethrin induced pronounced, dose-dependent alterations in neural fatty acid metabolism, including significant elevations in total fatty acids, saturated fatty acids, and polyunsaturated fatty acids. Medium and high doses increased multiple individual fatty acids, notably palmitic, stearic, oleic, linoleic and α-linolenic acids, as well as several very-long-chain saturated species. The observed fatty acid accumulation is consistent with possible impaired mitochondrial β-oxidation and redox imbalance previously reported for deltamethrin-exposed organisms, and suggests the emergence of a lipotoxic neural environment that may compromise membrane integrity, myelination and synaptic function. Our findings reveal fatty acid dysregulation as a sensitive mechanistic endpoint of pyrethroid neurotoxicity and highlight the importance of incorporating sublethal biochemical biomarkers into pesticide risk assessment frameworks aimed at protecting pollinator health.
Mackei et al. (Sat,) studied this question.