Ants act as keystone species in terrestrial ecosystems, providing important ecosystem services. The large-scale production and application of GO constitute a predominant contributor to its inevitable environmental dispersion. Most GO toxicity studies have focused on plants, animals, and microorganisms, with limited research on ground-dwelling ants. In the study, we used Camponotus japonicus as a model to investigate the toxic effects of GO on ants by integrating physiological characteristics, gut microbiota and transcriptome profiling. Results showed that GO exposure induced mitochondrial dysfunction, as evidenced by mitochondrial ROS accumulation and elevated mitochondrial membrane permeability. Physiological assessments revealed that GO exposure induced oxidative stress. Specifically, GO treatment significantly suppressed superoxide dismutase (SOD) and catalase (CAT) activities, while enhancing peroxidase (POD) and carboxylesterase (CarE) activities and increasing the levels of malondialdehyde (MDA) and trehalose. Gut microbiota analyses showed that GO remarkably reduced the relative abundance of beneficial bacterial symbionts (e.g., Candidatus Blochmannia) and destabilized the whole community structure. Furthermore, transcriptome profiling revealed 680 differentially expressed genes (DEGs) in the ants after GO exposure, most of which were significantly enriched in pathways associated with oxidative phosphorylation. This study suggests that GO may compromise ant-mediated ecosystem function and provides a reference for understanding the environmental risks of GO. Our findings also offer new insights for protecting the ecosystem services of ants.
Lei et al. (Fri,) studied this question.