# The role of sodium pyruvate in mitigating the cytotoxic effects of vanadium on CHO-K1 cells

**Authors:** Iwona Zwolak, Ewa Wnuk, Elżbieta Kochanowicz

PMC · DOI: 10.1038/s41598-025-09606-7 · Scientific Reports · 2025-07-05

## TL;DR

This study shows that sodium pyruvate can reduce the harmful effects of vanadium on CHO-K1 cells by protecting against cell damage and reducing necrosis.

## Contribution

The study demonstrates that exogenous pyruvate mitigates vanadium-induced cytotoxicity in a cell-specific manner.

## Key findings

- Vanadyl sulfate caused morphological changes, reduced ATP, and glutathione levels in CHO-K1 cells.
- Sodium pyruvate significantly reduced vanadium-induced necrosis and cytotoxicity in CHO-K1 cells.
- The protective effect of pyruvate was also observed in NIH/3T3 cells, indicating it is not cell-specific.

## Abstract

Vanadium is a hazardous, pro-oxidant element that contributes to environmental pollution and has been reported as a risk factor for human health through occupational or environmental exposure. Pyruvate, on the other hand, is a natural alpha-keto acid with exceptional antioxidant and cytoprotective properties. Therefore, the aim of this study was to evaluate the mitigating effect of exogenous pyruvate against vanadium-induced toxicity in cultured Chinese hamster ovary (CHO)-K1 cells. To this end, CHO-K1 cells were exposed to 100 μM vanadyl sulfate (VOSO4) for 24 h in the presence of 4.5 and 8 mM sodium pyruvate. Cell proliferation and morphological changes, cellular ATP levels, antioxidant stress (GSH) levels and apoptosis markers (caspase 3, 9, annexin V binding) were assessed to investigate the effect of sodium pyruvate on VOSO4-induced damage in CHO-K1 cells. The results showed that VOSO4 induced morphological changes, inhibited cell proliferation, decreased cellular ATP and reduced glutathione levels. Co-treatment of VOSO4-intoxicated CHO-K1 cells with sodium pyruvate significantly reduced these cytotoxic effects. Analysis of apoptosis and necrosis showed that VOSO4 slightly induced apoptosis and necrosis, and exogenous pyruvate inhibited the cytotoxicity of the tested vanadium dose in CHO-K1 cells, mainly by reducing the necrosis effect. The cytoprotective effect of exogenous pyruvate was also confirmed in normal mouse fibroblast (NIH/3T3) cells demonstrating that the protective properties of pyruvate are not cell specific.

## Linked entities

- **Chemicals:** vanadium (PubChem CID 23990), pyruvate (PubChem CID 107735), sodium pyruvate (PubChem CID 23662274), vanadyl sulfate (PubChem CID 34007), glutathione (PubChem CID 124886)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** necrosis (MESH:D009336), cytotoxic (MESH:D064420)
- **Chemicals:** ATP (MESH:D000255), Pyruvate (MESH:D019289), Vanadium (MESH:D014639), GSH (MESH:D005978), VOSO (-)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]
- **Cell lines:** NIH/3T3 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0594), CHO)-K1 — Cricetulus griseus (Chinese hamster), Spontaneously immortalized cell line (CVCL_0213)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12227759/full.md

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Source: https://tomesphere.com/paper/PMC12227759