The triggered antioxidant response and corresponding metabolomics expression of Caenorhabditis elegans for chronic exposure to moxifloxacin and trace copper

As the terminal management for evaluating the engineering effectiveness of antibiotics production and utilization, the toxic effects of moxifloxacin (MOX) and trace concentration of Cu²⁺ (MOX-Cu) on Caenorhabditis elegans (C. elegans) were investigated at physiological, biochemical, and molecular level. Although the stimulate effects were observed after prolonged exposure (72 h) to MOX (0.2-2.0 mg/L), the expressions of HSPs, ace genes, and daf-16 were inhibited, indicating its adverse impact on cellular health, locomotion behaviors, and antioxidant defense of C. elegans. Similarly, the down-regulation of oxidative stress (sod-1 and daf-16) and cell damage (HSPs) related genes and the up-regulation of apoptosis-related genes (cep-1 and ape-1) indicated the oxidative stress and genotoxicity after prolonged exposure to MOX-Cu. For the chronic exposure (10 days) to MOX, the level of ROS was reduced due to the increased expressions of daf-16, sod-3, and hsp-16, accompanied with and the down-regulation of cep-1. Meanwhile, at the exposure to MOX-Cu, the levels of ROS and lipofuscin were decreased due to the up-regulation of sod-1 and daf-16, and the antioxidant defense was promoted and confirmed by the increase of amino acids and their related metabolic pathways. These results can provide a theoretical basis for the toxicity evaluation of typical antibiotics (MOX) that co-existing with trace heavy metals in natural environment media and bioresources processes.