The mutagenic and clastogenic activities of vanadium-oxide (1314347) (V2O3), vanadyl-sulfate (27774136) (VOSO4), and ammonium- metavanadate (7803556) (NH4VO3) in inducing sister chromatid exchange (SCE) and chromosomal aberrations (CAb) were assessed in Chinese-hamster-ovary (CHO) cells. Exponentially growing cells were incubated with different concentrations of the test samples in order to establish the 50% toxic concentration (TC50). Vanadium compounds at high doses were noted to be cytotoxic to the CHO cells. The TC50s were approximately 25, 23, and 16 micrograms elemental vanadium per milliliter for V2O3, VOSO4, and NH4VO3, respectively. Morphological cytopathic effects observed at vanadium concentrations greater than the TC50 included rounding of cells and loss of nucleolar definition. At doses one fiftieth to one quarter the TC50, the compounds were able to induce significant increases in SCE frequency with or without the addition of rat hepatic S9 mix. The compounds also induced CAb in the cells at doses close to the TC50s. Analysis of individual aberrations revealed that gaps, breaks and exchanges were prevalent and increased with vanadium concentrations. The authors conclude that vanadium salts are both mutagenic and clastogenic in cultured CHO cells. The biochemical mechanism by which vanadium induces SCE and CAb is unclear but may be related to the effects of vanadium on DNA repair enzymes and protein synthesis.
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