Exposure to vanadium has been associated with deleterious effects on the central nervous system in animals and humans. Although vanadium-derived pro-oxidant species were reported to be involved in vanadium-mediated neurotoxicity, the ability of this metal to induce oxidative stress markers in glial cells remains to be elucidated. In this study, we investigated the cytotoxicity and the generation of reactive oxygen species (ROS) and nitric oxide (NO) by mouse primary astrocytes after treatment with vanadyl sulfate (VOSO4 ) at concentrations of 20, 50, 100, 200, and 500 μM. The resazurin assay revealed that treatment with VOSO4 for 24 and 48 h at concentrations of 50 and 100 μM, respectively, or higher substantially induced astrocytic cytotoxicity. Intracellular ROS increased after 6-h exposure to the lowest concentration tested (20 μM VOSO4 ) and tended to intensify after 24- and 48-h treatments reaching significant values for 20 and 500 μM VOSO4 . In turn, NO production in the examined cells was elevated after exposure to all concentrations at the 6-, 24-, and 48-h incubation periods. Our study demonstrated the ability of VOSO4 to induce H2 O2 generation in cell-free DMEM/F12 medium. The H2 O2 levels were in the micromolar range (up to 5 μM) and were detected mostly during the first few minutes after VOSO4 addition, suggesting that the generated H2 O2 could not induce toxic effects on the cells. Taken together, these results show VOSO4 induced cytotoxicity in primary astrocyte cells, which may have resulted from vanadyl-stimulated intracellular ROS and NO generation in these cells.
Keywords: astrocytes; cytotoxicity; oxidative stress markers; vanadyl sulfate.
© 2020 John Wiley & Sons, Ltd.