Multi-omics analyses reveal molecular mechanisms for the antagonistic toxicity of carbon nanotubes and ciprofloxacin to Escherichia coli.

With the increasing production and application, engineered nanomaterials (ENMs) are being discharged into the environment, where they can interact with co-existing contaminants, causing complicated joint toxicity to organisms that needs to be studied. The case study of ENMs-contaminant joint toxicity and the understanding of relative mechanisms are very insufficient, particularly the mechanisms of molecular interactions and governing processes. Herein, a typical ENMs, carbon nanotubes (CNTs, 0-60 mg/L), and a common antibiotic, ciprofloxacin (CIP, 0-900 mg/L), were selected as the analytes. Their joint toxicity to a model microbe Escherichia coli was specifically investigated via biochemical, transcriptomics, and metabolomics approaches. The result revealed an antagonistic effect on growth inhibition between CNTs and CIP. Mitigations in cell membrane disruption and oxidative stress were involved in the antagonistic action. CIP (48.8-244 mg/L) decreased the bioaccumulation of CNTs (7.2 mg/L) via reducing cell-surface hydrophobicity and hindering the bio-nano interaction, which could attenuate the toxicity of CNTs to bacteria. CNTs (7.2 and 14.4 mg/L) alleviated the disturbance of CIP (122 and 244 mg/L) to gene expressions especially related to nitrogen compound metabolism, oxidoreductase activity, and iron-sulfur protein maturation, probably through relieving the CIP-induced inhibition of DNA gyrase activity. Further, CNTs (7.2 and 14.4 mg/L) offset the impact of CIP (122 and 244 mg/L) on bacterial metabolome via the regulation of biosynthesis of unsaturated fatty acids and metabolisms of some amino acids and glutathione. The findings shed new light on the molecular mechanisms by which ENMs present joint effect on contaminant toxicity, and provide important information for risk assessments of CNTs and fluoroquinolones in the environment.