Premature chromatid separation and altered proliferation of human leukocytes treated with vanadium (III) oxide

Abstract

Vanadium is a widely distributed metal in the Earth’s surface and is released into the environment by either natural or anthropogenic causes. Vanadium (III) oxide (V₂O₃) is present in the environment, and many organisms are exposed to this compound; however, its effects at the cellular and genetic levels are still unknown. Therefore, in this study, the ability of V₂O₃ to induce chromosomal damage and impair cell proliferation was tested on human leukocytes in vitro. The cultures cells were treated for 48 h with different concentrations 2, 4, 8 or 16 μg/mL of V₂O₃, and we use the sister chromatid exchange’s (SCE) test and the viability assay to evaluate the effects.

In the results, no change was observed in either the viability or the frequency of SCE; however, a significant increase was observed in the incidence of premature chromatid separation (PCS), and a decrease was observed in both the mitotic index (MI) and the replication index (RI). Therefore, it can be suggested that V₂O₃ induces a genotoxic effect at the centromere level, indicating that it is a cause of aneuploidy that is capable of altering cell cycle progression.

Keywords:

• Vanadium (III) oxide
• lymphocytes
• sister chromatid exchange
• citostatic
• premature chromatid separation

Acknowledgements

This wok was supported by Universidad Nacional Autónoma de México project PAPIIT IN224916. Mateos-Nava thanks Posgrado en Ciencias Biológicas, UNAM, and to the scholarship CONACYT-210454.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.