We attempted to determine the level and form of selenium (Se) that yielded the maximum Se status of yeast cells, for their evaluation as a source of Se for chemopreventive action. The influence of various Se concentrations from organic (selenomethionine) and inorganic (sodium selenite) Se compounds on growth pattern and cell viability and the alterations in the antioxidant enzyme system of yeast were evaluated. A continuous decrease in cell and colony-forming units counts was observed with increasing concentrations of Se from either source. Increasing Se status of yeast cells was found with increasing concentrations of Se with both forms, with much greater uptake for organic Se at maximum Se concentrations. A continuous increase in glutathione peroxidase (GSH-Px) activity with increasing Se concentrations in both forms revealed an active Se response in terms of antioxidant activity, with a more pronounced percentage increase with selenomethionine. A highly significant increase in total glutathione was observed with selenomethionine supplementation, compared with sodium selenite. A decreasing trend in reduced glutathione was observed with increasing organic or inorganic Se concentrations. An increasing trend in glutathione-S-transferase activity was observed with increasing Se concentrations for both forms. Significantly higher values of glutathione-S-transferase were associated with the organic form at higher Se concentrations. There was normal activity of Se in mammalian cells. The results showed that an organic Se source more greatly enhances the Se status of yeast cells and hence could help in chemoprevention if consumed by the population.
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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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