Genotoxicity of vanadium compounds in yeast and cultured mammalian cells

Abstract

The ability of vanadium compounds to induce genetic activity was investigated in D7 and D61M strains of Saccharomyces cerevisiae and in Chinese hamster V79 cell line. In our previous work, ammonium metavanadate (pentavalent form, V5) induced mitotic gene conversion and point reverse mutation in the D7 strain of yeast. The genotoxicity was reduced by the presence of S9 fraction, which probably reduced pentavalent vanadium to the tetravalent form. In the present study, vanadyl sulfate (tetravalent form, V4) induced no convertants and revertants in yeast cells harvested from stationary growth phase. With yeast cells from logarithmic growth phase, which contain high levels of cytochrome P-450, a significant increase in genetic effects was observed. Further experiments, performed by treating cells harvested from logarithmic growth phase in the presence of cytochrome P-450 inhibitors, indicated that the monooxygenase system influenced the genotoxicity of metavanadate while the genetic activity of vanadyl remained unaffected. Aneuploidy effect in the D61M strain of Saccharomyces cerevisiae was induced by either V5 or V4, confirming that vanadium compounds are potentially antitubulin agents in eukaryotic cells. Although these compounds are very toxic in V79 cells, no mutagenic effect was observed in the presence or in the absence of S9 fraction.

Genotoxicity of 11 heavy metals detected as food contaminants in two human cell lines

“…Using the H2AX assay, we obtained similar results for VCl 3 . We confirmed the results of previous studies in which no increase in the incidence of DNA strand breaks (comet assay), oxidative stress, sister chromatid exchange or mutagenesis was observed with this chemical [Galli et al, ; Villani et al, ; Manjanatha et al, ].…”

In vitro embryotoxicity testing of metals for dental use by differentiation of embryonic stem cell test

“…Our test results for tin indicated a weak embryotoxicity similar to antimony. Vanadium's mutagenicity has been previously indicated (Galli et al . 1991).…”

Opinion of the Scientific Panel on Dietetic products, nutrition and allergies [NDA] related to the Tolerable Upper Intake Level of Vanadium

“…Positive results were also obtained in the same test system with vanadyl sulfate (+4) at concentrations from 26.1 to 68.5 µg/mL, only in experiments with cells from logarithmic growth phase (Galli et al, 1991). In the same study, both ammonium metavanadate (0.47-0.58 µg/mL) and vanadyl sulfate (1.22-1.63 µg/mL) induced mitotic aneuploidy in the S. cerevisiae strain D6.1M.…”

“…In Chinese hamster V79 cells, no induction of forward mutations at the hprt locus was observed after treatment with vanadyl sulfate (+4) (0.081-0.81 µg/mL, both in the presence or in the absence of metabolic activation (Galli et al, 1991), or after treatment with vanadium pentoxide (1-3 µg/mL) in the absence of metabolic activation (Zhong et al, 1994). In experiments without exogenous metabolic activation, ammonium metavanadate, at low noncytotoxic concentrations (up to 0.58 ng/mL), increased the frequency of mutations at the hprt locus in V79 cells, and, at higher concentrations (0.585 µg/mL), at the bacterial gpt gene in transgenic G12 cells (Cohen et al, 1992).…”