ReviewArsenic and selenium toxicity and their interactive effects in humans

- As and Se are both carcinogens and anticarcinogens.
- Reactive oxygen species play a role in their toxicity.
- Glutathione and S-adenosylmethionine are important in their detoxification.
- Synergistic and antagonistic effects exist between As and Se toxicity.
- Formation of [(GS)2AsSe]− reduces both As and Se toxicity.

Arsenic (As) and selenium (Se) are unusual metalloids as they both induce and cure cancer. They both cause carcinogenesis, pathology, cytotoxicity, and genotoxicity in humans, with reactive oxygen species playing an important role. While As induces adverse effects by decreasing DNA methylation and affecting protein 53 expression, Se induces adverse effects by modifying thioredoxin reductase. However, they can react with glutathione and S-adenosylmethionine by forming an As-Se complex, which can be secreted extracellularly. We hypothesize that there are two types of interactions between As and Se. At low concentration, Se can decrease As toxicity via excretion of As-Se compound [(GS3)2AsSe]−, but at high concentration, excessive Se can enhance As toxicity by reacting with S-adenosylmethionine and glutathione, and modifying the structure and activity of arsenite methyltransferase. This review is to summarize their toxicity mechanisms and the interaction between As and Se toxicity, and to provide suggestions for future investigations.

Synergistic and antagonistic relation between As and Se toxicity in humans.