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.