Cadmium exposure induces acute and delayed physiological effects in bumblebee (Bombus terrestris) gynes.

Cadmium (Cd), a potent environmental contaminant, persists widely in the environment and threatens global ecosystems. However, the underlying mechanisms of its acute and delayed toxicity effects on pollinating insects still remains elusive. Here, we systematically investigated whether and how environmentally relevant concentrations of Cd exposure impose acute and delayed toxic effects on bumblebees. Seven day exposure of environmentally relevant Cd concentration to gynes exhibited acute toxic effects, impairing their learning and memory capacity. Nutrient reserves were impaired and their growth and development were hindered, thereby reducing mating performance. Notably, Cd exposure exhibited a delayed effect on metabolism, disrupting nutrient homeostasis in queen's diapause and leading to reduced survival. Transcriptome profiling analysis showed that the expression of genes involved in DNA damage response and reactive oxygen species (ROS) clearance was perturbed upon Cd exposure. Consistently, ROS accumulation and increased DNA damage were observed in the fat body of Cd-exposed gynes. Importantly, oral administration of antioxidant, N-acetylcysteine (NAC), effectively ameliorated the adverse impacts induced by Cd exposure. Therefore, our work unveils the main cause of the multidimensional acute/delayed physiological damages resulted from Cd exposure in gynes and discovers an effective therapeutics for Cd-exposed bumblebees. Thus, our study underscores the urgent need for regulatory consideration of heavy metal pollution for bumblebee conservation.