Mutagenic responses of nickel oxides and nickel sulfides in Chinese hamster V79 cell lines at the xanthine-guanine phosphoribosyl transferase locus.

Mutagenesis of several insoluble nickel compounds--crystalline nickel sulfide NiS, nickel subsulfide Ni3S2, nickel oxides (black and green) and soluble NiCl2 was studied in three Chinese hamster cell lines--at the hprt gene of the well-defined V79 cell line, and at gpt in two transgenic derivative cell lines G12 and G10. The transgenic cell line G12 responded very strongly to the insoluble Ni compounds, such that the gpt mutagenesis was at least 20 times higher than the spontaneous mutagenesis and in some experiments was even higher. In contrast the response of the G10 cells was much lower--the mutant frequencies only increased 2-3 times over the controls. In V79 cells, NiS and NiO (black) did not induce a mutagenic response at hprt. Soluble NiCl2 also exhibited no mutagenic activity in V79 cells and induced considerably lower activity than the insoluble compounds in the transgenic G12 cells. Following vitamin E pretreatment of G12 cells for 24 h prior to nickel exposure, increased cell survival was observed for several insoluble Ni compounds whereas vitamin E had no effect on NiCl2 cytotoxicity. With vitamin E pretreatment, significantly lower mutagenic responses in G12 cells were also noted for some insoluble Ni compounds, while no such effect was observed for NiCl2.