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

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.