Protective activity of pyruvate against vanadium-dependent cytotoxicity in Chinese hamster ovary (CHO-K1) cells.

With increasing human exposure to vanadium-containing compounds and growing concern over their impact on human health, identification of safe methods for efficient treatment of vanadium poisoning may be of value. In this study, using Chinese hamster ovary (CHO-K1) cells, we show that the toxicity of vanadyl sulphate (VOSO) is mitigated in the presence of sodium pyruvate. The exposure of CHO-K1 cells to 100 μM VOSO for 48 h induced significant cytotoxicity (measured with a resazurin assay) and elevation of the contents of malondialdehyde (MDA), a lipid peroxidation product, in the examined cells. When added simultaneously with VOSO to the culture medium, pyruvate (4.5 mM) reduced VOSO-mediated cytotoxicity by twofold and inhibited MDA formation. Phase-contrast microscopy confirmed that the general morphology of cell cultures treated with 100 μM VOSO and 4.5 mM pyruvate was improved compared to VOSO-only treated cells. The two-way analysis of variance revealed that the reduction of the adverse effects of VOSO in the presence of pyruvate was due to the independent action of pyruvate as well as antagonistic interaction between VOSO and pyruvate. From these data, it can be concluded that the pyruvate treatment may play a beneficial role in reducing vanadium-triggered health hazards.