Cellular glutathione (GSH) was implicated in tolerance to potentially toxic metal(loid)s using two strains of Saccharomyces cerevisiae, a wild-type (sigma 1278b) and a GSH-deficient mutant strain (gshA-2). Both yeast strains exhibited no significant difference in tolerance to tellurite, zinc, cobalt, copper, manganese, nickel and chromate. There was no marked influence of glutathione on the accumulation of Te, Co, Cu, and Mn, although the absence of cellular glutathione significantly increased the cellular content of Zn and Ni, but greatly decreased Cr content without significant alteration of tolerance. These results indicated the independence of cellular glutathione activity from tolerance to Te, Zn, Co, Cu, Mn, Ni, and Cr. However, involvement of glutathione in Zn, Ni and Cr uptake is possible. The glutathione-deficient strain displayed a high sensitivity to selenite and cadmium in comparison to the wild-type strain of S. cerevisiae. The minimum inhibitory concentrations of Se and Cd for the glutathione-deficient strain were 980 +/- 13 and 32 +/- 4 microM, respectively, whereas the wild strain tolerated up to 4080 +/- 198 microM Se and 148 +/- 5 microM Cd. A relationship between tolerance and reduced cellular content of both Se and Cd was also shown: the mutant strain accumulated approximately three-fold more Se and two-fold more Cd than that accumulated by the wild-type strain. This suggests an influence of GSH on cellular uptake of Se and Cd, and also directly confirms the protective action of such a cellular thiol compound against Se and Cd toxicity.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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