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<p>As the terminal management for evaluating the engineering effectiveness of antibiotics production and utilization, the toxic effects of moxifloxacin (MOX) and trace concentration of Cu<sup>2+</sup> (MOX-Cu) on <i>Caenorhabditis elegans</i> (<i>C. elegans</i>) were investigated at physiological, biochemical, and molecular level. Although the stimulate effects were observed after prolonged exposure (72&#xa0;h) to MOX (0.2-2.0&#xa0;mg/L), the expressions of HSPs, ace genes, and <i>daf-16</i> were inhibited, indicating its adverse impact on cellular health, locomotion behaviors, and antioxidant defense of <i>C. elegans</i>. Similarly, the down-regulation of oxidative stress (<i>sod-1</i> and <i>daf-16</i>) and cell damage (HSPs) related genes and the up-regulation of apoptosis-related genes (<i>cep-1</i> and <i>ape-1</i>) 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 <i>daf-16</i>, <i>sod-3</i>, and <i>hsp-16</i>, accompanied with and the down-regulation of <i>cep-1</i>. Meanwhile, at the exposure to MOX-Cu, the levels of ROS and lipofuscin were decreased due to the up-regulation of <i>sod-1</i> and <i>daf-16</i>, 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.</p> Graphical Abstract <p></p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月17日

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  • Lili Liu,
  • Yuxia Liu,
  • Mingqi Tang,
  • Manman Zhu,
  • Fangfang Wang,
  • Kuangfei Lin

摘要

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.

Graphical Abstract