This review describes nickel toxicity and nickel resistance mechanisms in fungi. Nickel toxicity in fungi is influenced by environmental factors such as pH, temperature and the existence of organic matter and other ions. We describe resistance mechanisms in nickel-resistant mutants of yeasts and filamentous fungi which were obtained by exposure to a mutagen or by successive culture in media containing increasing concentrations of nickel ion. Nickel resistance may involve: (1) inactivation of nickel toxicity by the production of extracellular nickel-chelating substances such as glutathione; (2) reduced nickel accumulation, probably by modification of a magnesium transport system; (3) sequestration of nickel into a vacuole associated with free histidine and involving Ni-insensitivity of vacuolar membrane H(+)-ATPase.

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Yeast cells carrying the CAD2 gene exhibit a resistance to cadmium. We cloned this gene and demonstrated that it was a mutated form derived from the gene of a putative copper-transporting ATPase (PCA1). By site-directed mutagenesis, it appeared that the mutation conferring cadmium resistance was a R970G-substitution in the C-terminal region of Pca1 protein. The intracellular cadmium level of cells carrying CAD2 was lower than that of cells carrying either PAC1 or delta cad2. Furthermore, cells with overexpression of CAD2 showed a much lower intracellular cadmium level than that of cells with a single-copy CAD2. From these results, we conclude that the Cad2 protein controls the intracellular cadmium level through an enhanced cadmium efflux system.

Suspension-cultured cells of azuki bean (Vigna angularis) as well as the original root tissues were hypersensitive to Cd (<10 μm). Repeated subculturings with a sublethal level of Cd (1–10 μm) did not affect the subsequent response of cells to inhibitory levels of Cd (10–100 μm). The azuki bean cells challenged to Cd did not contain phytochelatin (PC) peptides, unlike tomato (Lycopersicon esculentum) cells that have a substantial tolerance to Cd (>100 μm). Both of the cell suspensions contained a similar level of reduced glutathione (GSH) when grown in the absence of Cd. Externally applied GSH to azuki bean cells recovered neither Cd tolerance nor PC synthesis of the cells. Furthermore, enzyme assays in vitro revealed that the protein extracts of azuki bean cells had no activity converting GSH to PCs, unlike tomato. These results suggest that azuki bean cells are lacking in the PC synthase activity per se, hence being Cd hypersensitive. We concluded that the PC synthase has an important role in Cd tolerance of suspension-cultured cells.

When a Cd-resistant strain (301 N) and a Cd-sensitive strain (101 N ) of Saccharomyces cereuisiae were incubated in medium containing Cd2+, a large proportion of the cellular Cd2+ was found in the cytosol of strain 301 N, but not in that of strain 101N. Approximately 65% of the cellular Cd2+ was released from strain 301 N after treatment with chitosan, which affects cell membrane permeability. About 807; of the cellular Cd2+ released from strain 301 N by chitosan treatment was detected in a 30000-10000 molecular weight fraction prepared by ultrafiltration. The distribution of Cd2+ into the cytosol in strain 301N was inhibited in the presence of cycloheximide. The proportion of cellular Cu2+ or Zn2+ present in the cytosol after incubation with these ions was similar for the two strains (about 40"/,).