Food contamination with fipronil alters gene expression associated with foraging in Africanized honey bees.

Taking into consideration that bees can be contaminated by pesticides through the ingestion of contaminated floral resources, we can utilize genetic techniques to assess effects that are scarcely observed in behavioral studies. This study aimed to investigate the genetic effects of ingesting lethal and sublethal doses of the insecticide fipronil in foraging honey bees during two periods of acute exposure. Bees were exposed to fipronil through contaminated honey syrup at two dosages (LD50 = 0.19 µg/bee; LD50/100 = 0.0019 µg/bee) and for two durations (1 and 4 h). Following exposure, we measured syrup consumption per bee, analyzed the transcriptome of bee brain tissue, and identified differentially expressed genes (DEGs), categorizing them functionally based on gene ontology (GO). The results revealed a significant genetic response in honey bees after exposure to fipronil, regardless of the dosage used. Fipronil affected various metabolic, transport, and cellular regulation pathways, as well as detoxification processes and xenobiotic substance detection. Additionally, the downregulation of several DEGs belonging to the olfactory-binding protein (OBP) family was observed, suggesting potential physiological alterations in bees that may lead to disoriented behaviors and reduced foraging efficiency.

Intake of imidacloprid in lethal and sublethal doses alters gene expression in Apis mellifera bees.

Bees are important pollinators for ecosystems and agriculture; however, populations have suffered a decline that may be associated with several factors, including habitat loss, climate change, increased vulnerability to diseases and parasites and use of pesticides. The extensive use of neonicotinoids, including imidacloprid, as agricultural pesticides, leads to their persistence in the environment and accumulation in bees, pollen, nectar, and honey, thereby inducing deleterious effects. Forager honey bees face significant exposure to pesticide residues while searching for resources outside the hive, particularly systemic pesticides like imidacloprid. In this study, 360 Apis mellifera bees, twenty-one days old (supposed to be in the forager phase) previously marked were fed syrup (honey and water, 1:1 m/v) containing a lethal dose (0.081 µg/bee) or sublethal dose (0.00081 µg/bee) of imidacloprid. The syrup was provided in plastic troughs, with 250 µL added per trough onto each plastic Petri dish containing 5 bees (50 µL per bee). The bees were kept in the plastic Petri dishes inside an incubator, and after 1 and 4 h of ingestion, the bees were euthanised and stored in an ultra-freezer (-80 °C) for transcriptome analysis. Following the 1-h ingestion of imidacloprid, 1516 genes (73 from lethal dose; 1509 from sublethal dose) showed differential expression compared to the control, while after 4 h, 758 genes (733 from lethal dose; 25 from sublethal) exhibited differential expression compared to the control. All differentially expressed genes found in the brain tissue transcripts of forager bees were categorised based on gene ontology into functional groups encompassing biological processes, molecular functions, and cellular components. These analyses revealed that sublethal doses might be capable of altering more genes than lethal doses, potentially associated with a phenomenon known as insecticide-induced hormesis. Alterations in genes related to areas such as the immune system, nutritional metabolism, detoxification system, circadian rhythm, odour detection, foraging activity, and memory in bees were present after exposure to the pesticide. These findings underscore the detrimental effects of both lethal and sublethal doses of imidacloprid, thereby providing valuable insights for establishing public policies regarding the use of neonicotinoids, which are directly implicated in the compromised health of Apis mellifera bees.