ArticleEnvironmental science and pollution research international2024
Changes in the proteome of Apis mellifera acutely exposed to sublethal dosage of glyphosate and imidacloprid.
Article in Environmental science and pollution research international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Renaming the 'OS-D/CSP' Family (Part 2): '4-Cysteine Soluble Proteins' (4CSPs)-Intracellular Functions.Insects · 2026Review
- Differential expression of neuronal function genes follows a tissue-specific temporal dynamic during Deformed Wing Virus infection in honey bees.Scientific reports · 2026Article
- Long Non-Coding RNA LOC113219358 Regulates Immune Responses inInternational journal of molecular sciences · 2025Article
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7 authors.
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Abstract
Uncontrolled use of pesticides has caused a dramatic reduction in the number of pollinators, including bees. Studies on the effects of pesticides on bees have reported effects on both metabolic and neurological levels under chronic exposure. In this study, variations in the differential expression of head and thorax-abdomen proteins in Africanized A. mellifera bees treated acutely with sublethal doses of glyphosate and imidacloprid were studied using a proteomic approach. A total of 92 proteins were detected, 49 of which were differentially expressed compared to those in the control group (47 downregulated and 2 upregulated). Protein interaction networks with differential protein expression ratios suggested that acute exposure of A. mellifera to sublethal doses of glyphosate could cause head damage, which is mainly associated with behavior and metabolism. Simultaneously, imidacloprid can cause damage associated with metabolism as well as, neuronal damage, cellular stress, and impairment of the detoxification system. Regarding the thorax-abdomen fractions, glyphosate could lead to cytoskeleton reorganization and a reduction in defense mechanisms, whereas imidacloprid could affect the coordination and impairment of the oxidative stress response.
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