# Copper-Induced Thyroid Disruption and Oxidative Stress in Schizopygopsis younghusbandi Larvae

**Authors:** Liqiao Zhong, Chi Zhang, Fei Liu, Haitao Gao, Dengyan Di, Fan Yao, Baoshan Ma, Mingdian Liu, Xinbin Duan

PMC · DOI: 10.3390/antiox15010112 · Antioxidants · 2026-01-15

## TL;DR

This study shows that copper exposure harms the thyroid and antioxidant systems in fish larvae from Lhasa River, affecting their growth and survival.

## Contribution

The study reveals novel insights into copper's toxic effects on thyroid function and oxidative stress in a native Lhasa River fish species.

## Key findings

- Copper exposure reduced thyroid hormone levels and altered thyroid hormone synthesis gene expression in fish larvae.
- Copper increased antioxidant enzyme activity and lipid peroxidation while decreasing glutathione content in larvae.
- Copper exposure caused dose- and time-dependent developmental toxicity in S. younghusbandi larvae.

## Abstract

In recent years, heavy metal emissions in Lhasa have been increasing, which has an impact on the local water environment. The negative effects of copper (Cu2+) on aquatic ecosystems have attracted much attention, as even low concentrations of Cu2+ can exert toxic effects on aquatic organisms. However, the impact of Cu2+ on native fish species from the Lhasa River remains poorly understood. In this study, Schizopygopsis younghusbandi (S. younghusbandi) larvae were exposed to Cu2+ at concentrations of 0. 5, 5, 50, and 500 μg/L for 7 or 14 days to evaluate its toxic effects on thyroid function and the antioxidant system. The results indicate that whole-body total thyroxine (T4) and triiodothyronine (T3) levels were significantly decreased following Cu2+ exposure. This decrease was accompanied by a marked increase in dio1 and dio2 gene expression and decreased expression of thyroid hormone synthesis genes (nis, tg, ttf1 and pax8) after exposure to Cu2+. Furthermore, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR) and the content of lipid peroxidation were increased, while the content of glutathione (GSH) was decreased. In addition, the survival rates and body lengths of S. younghusbandi larvae were significantly reduced following 7- and 14-day Cu2+ exposure. The Integrated Assessment of Biomarker Response (IBR) analysis further revealed dose- and time-dependent effects of Cu2+ on the larvae. In conclusion, the findings demonstrate that Cu2+ exposure induced disruption of thyroid endocrine and antioxidant systems and caused developmental toxicity in S. younghusbandi larvae.

## Linked entities

- **Genes:** DIO1 (iodothyronine deiodinase 1) [NCBI Gene 1733], DIO2 (iodothyronine deiodinase 2) [NCBI Gene 1734], SLC5A5 (solute carrier family 5 member 5) [NCBI Gene 6528], TG (thyroglobulin) [NCBI Gene 7038], TTF1 (transcription termination factor 1) [NCBI Gene 7270], PAX8 (paired box 8) [NCBI Gene 7849]
- **Chemicals:** copper (PubChem CID 23978), Cu2+ (PubChem CID 27099)
- **Species:** Schizopygopsis younghusbandi (taxon 263521)

## Full-text entities

- **Genes:** DIO2 (iodothyronine deiodinase 2) [NCBI Gene 1734] {aka 5DII, D2, DIOII, SELENOY, SelY, TXDI2}, SLC5A5 (solute carrier family 5 member 5) [NCBI Gene 6528] {aka NIS, TDH1}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, CAT (catalase) [NCBI Gene 847], TTF1 (transcription termination factor 1) [NCBI Gene 7270] {aka TTF-1, TTF-I}, DIO1 (iodothyronine deiodinase 1) [NCBI Gene 1733] {aka 5DI, THMA2, TXDI1}, PAX8 (paired box 8) [NCBI Gene 7849] {aka PAX-8}, GSR (glutathione-disulfide reductase) [NCBI Gene 2936] {aka CNSHA10, GR, GSRD, HEL-75, HEL-S-122m}
- **Diseases:** developmental toxicity (MESH:D064420), Thyroid Disruption (MESH:D013966)
- **Chemicals:** T3 (MESH:D014284), Cu2+ (-), T4 (MESH:D013974), lipid (MESH:D008055), GSH (MESH:D005978), heavy metal (MESH:D019216), Copper (MESH:D003300)
- **Species:** Schizopygopsis younghusbandi (species) [taxon 263521]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12838212/full.md

## References

59 references — full list in the complete paper: https://tomesphere.com/paper/PMC12838212/full.md

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Source: https://tomesphere.com/paper/PMC12838212