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

**Authors:** Lili Liu, Yuxia Liu, Mingqi Tang, Manman Zhu, Fangfang Wang, Kuangfei Lin

PMC · DOI: 10.1186/s40643-026-01033-4 · Bioresources and Bioprocessing · 2026-03-17

## TL;DR

This study examines how moxifloxacin and trace copper affect the health and antioxidant responses of C. elegans over time.

## Contribution

The study reveals new insights into the combined toxic effects of moxifloxacin and trace copper on C. elegans at multiple biological levels.

## Key findings

- Prolonged exposure to moxifloxacin inhibits genes related to cellular health and antioxidant defense in C. elegans.
- Chronic exposure to moxifloxacin and copper reduces ROS levels and promotes antioxidant defenses through gene regulation.
- The study identifies specific gene and metabolic responses to chronic exposure of moxifloxacin and trace copper in C. elegans.

## Abstract

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.

The online version contains supplementary material available at 10.1186/s40643-026-01033-4.

## Linked entities

- **Genes:** hsp70-1 (heat shock protein 70-1) [NCBI Gene 3879515], ACE (angiotensin I converting enzyme) [NCBI Gene 1636], daf-16 (Forkhead box protein O) [NCBI Gene 172981], SOD1 (superoxide dismutase 1) [NCBI Gene 6647], CNTRL (centriolin) [NCBI Gene 11064], APEX1 (apurinic/apyrimidinic endodeoxyribonuclease 1) [NCBI Gene 328], SOD3 (superoxide dismutase 3) [NCBI Gene 6649], hsp16 (heat shock protein Hsp16) [NCBI Gene 2540977]
- **Chemicals:** moxifloxacin (PubChem CID 152946), Cu2+ (PubChem CID 27099)
- **Species:** Caenorhabditis elegans (taxon 6239)

## Full-text entities

- **Genes:** act-5 (Actin) [NCBI Gene 176793], sod-3 (Superoxide dismutase) [NCBI Gene 181748], cep-1 (Transcription factor cep-1) [NCBI Gene 172616], daf-16 (Forkhead box protein O) [NCBI Gene 172981], sod-1 (Superoxide dismutase) [NCBI Gene 174141], ape-1 (Apoptotic enhancer 1 protein) [NCBI Gene 179601], hsp-16.48 (Heat shock protein Hsp-16.48/Hsp-16.49) [NCBI Gene 179287], gst-4 (Glutathione S-transferase 4) [NCBI Gene 177886], ace-4 (Carboxylic ester hydrolase) [NCBI Gene 175074], ace-1 (Acetylcholinesterase 1) [NCBI Gene 181706], ace-2 (Carboxylic ester hydrolase) [NCBI Gene 171905], ace-3 (Carboxylic ester hydrolase) [NCBI Gene 175076], hsp-16.1 (Heat shock protein Hsp-16.1/Hsp-16.11) [NCBI Gene 179286], hsp-16.2 (Heat shock protein hsp-16.2;SHSP domain-containing protein) [NCBI Gene 178659]
- **Diseases:** locomotion impairments (MESH:D020233), neurological damage (MESH:D020196), coronavirus disease 2019 (MESH:D000086382), neurobehavioral deficit (MESH:D019954), tumor suppressor (OMIM:601308), neurotoxic (MESH:D020258), toxicity (MESH:D064420), Head thrashes (MESH:D006258)
- **Chemicals:** lysine (MESH:D008239), potassium phosphate (MESH:C013216), apigenin (MESH:D047310), ornithine (MESH:D009952), acetonitrile (MESH:C032159), glutathione (MESH:D005978), amino acid (MESH:D000596), glutamate (MESH:D018698), Fluoroquinolone (MESH:D024841), methanol (MESH:D000432), metal (MESH:D008670), Cu (MESH:D003300), proline (MESH:D011392), NaCl (MESH:D012965), MOX (MESH:D000077266), H2O (MESH:D014867), isopropyl alcohol (MESH:D019840), Serine (MESH:D012694), cholesterol (MESH:D002784), CAS: 7758-99-8 (-), norfloxacin (MESH:D009643), purine (MESH:C030985), CAS (MESH:D002118), KCl (MESH:D011189), heavy metals (MESH:D019216), Glutamine (MESH:D005973), Copper sulfate pentahydrate (MESH:D019327), oxygen (MESH:D010100), methionine (MESH:D008715), Lipofuscin (MESH:D008062), Arginine (MESH:D001120), enrofloxacin (MESH:D000077422), levamisole (MESH:D007978), NaOH (MESH:D012972), agar (MESH:D000362), K (MESH:D011188), TRIzol (MESH:C411644), pyridone (MESH:D011728)
- **Species:** Ceriodaphnia dubia (species) [taxon 117530], Escherichia coli (E. coli, species) [taxon 562], Caenorhabditis elegans (species) [taxon 6239], Microcystis aeruginosa (species) [taxon 1126], Uncaria tomentosa (species) [taxon 128375], Lampsilis siliquoidea (species) [taxon 52396], Danio rerio (leopard danio, species) [taxon 7955], Allium cepa (onion, species) [taxon 4679], C. elegans [taxon 328850], Homo sapiens (human, species) [taxon 9606], Daphnia magna (species) [taxon 35525]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12996479/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12996479/full.md

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Source: https://tomesphere.com/paper/PMC12996479