Honey bee Apis mellifera L. responses to oxidative stress induced by pharmacological and pesticidal compounds

Abstract

The western honey bee, Apis mellifera L., is a eusocial insect that plays a significant role in ecosystem balances and the pollination of plants and food crops. Honey bees face multiple biotic and abiotic stressors, such as pathogens, diseases, chemical pesticides, and climate change, which all contribute to honey bee colony loss. This study investigated the impacts of multiple pharmacological and pesticidal molecules on honey bee survival and gene regulation responses. In an 11-day cage experiment, sublethal doses of tunicamycin, thapsigargin, metformin, paraquat, hydrogen peroxide, and imidacloprid were administered to newly emerged sister bees. Daily treatment consumption and mortality were recorded, as well as the transcription expression of 12 major genes ( AChE-2 , Apisimin , Apidaecin , mrjp1 , Sodq , cp450 , SelT , SelK , Ire1 , Xbp1 , Derl-1 , and Hsc70 ), some of which are markers of oxidative and endoplasmic reticulum (ER) stresses in honey bees. At day 9 of the treatments, protein damage was quantified in caged bees. A Kaplan–Meier model indicated significant ( p < 0.001) toxicological effects of paraquat, H 2 O 2 , and tunicamycin on bee survivorship compared with controls with better survival for other molecules. Post-ingestive aversion responses were recorded only for tunicamycin, hydrogen peroxide, and imidacloprid. Nonetheless, significantly higher protein damage on day 9 was identified only in bees exposed to paraquat and imidacloprid. Some antioxidant genes were significantly regulated vis-à-vis specific treatments. Our results reveal age-related regulation of other major genes with significant inter-gene positive correlations.