Effects of Sodium Pyruvate on Vanadyl Sulphate-Induced Reactive Species Generation and Mitochondrial Destabilisation in CHO-K1 Cells.

Vanadium is ranked as one of the world's critical metals considered important for economic growth with wide use in the steel industry. However, its production, applications, and emissions related to the combustion of vanadium-containing fuels are known to cause harm to the environment and human health. Pyruvate, i.e., a glucose metabolite, has been postulated as a compound with multiple cytoprotective properties, including antioxidant and anti-inflammatory effects. The aim of the present study was to examine the antioxidant potential of sodium pyruvate (4.5 mM) in vanadyl sulphate (VOSO)-exposed CHO-K1 cells. Dichloro-dihydro-fluorescein diacetate and dihydrorhodamine 123 staining were performed to measure total and mitochondrial generation of reactive oxygen species (ROS), respectively. Furthermore, mitochondrial damage was investigated using MitoTell orange and JC-10 staining assays. We demonstrated that VOSO alone induced a significant rise in ROS starting from 1 h to 3 h after the treatment. Additionally, after 24 and 48 h of exposure, VOSO elicited both extensive hyperpolarisation and depolarisation of the mitochondrial membrane potential (MMP). The two-way ANOVA analysis of the results showed that, through antagonistic interaction, pyruvate prevented VOSO-induced total ROS generation, which could be observed at the 3 h time point. In addition, through the independent action and antagonistic interaction with VOSO, pyruvate provided a pronounced protective effect against VOSO-mediated mitochondrial toxicity at 24-h exposure, i.e., prevention of VOSO-induced hyperpolarisation and depolarisation of MMP. In conclusion, we found that pyruvate exerted cytoprotective effects against vanadium-induced toxicity at least in part by decreasing ROS generation and preserving mitochondrial functions.