✍ Scribed by Regina Brigelius-Flohé
No coin nor oath required. For personal study only.
An adequate selenium (Se) status has for long been considered to prevent the development of various forms of cancer. However, underlying molecular mechanisms remained unknown. In mammals, selenium exerts its functions as selenocysteine incorporated into selenoproteins. Therefore, Se compounds can either act as Se source for selenoproteins or, depending on their chemical forms, in distinct ways. Most potent chemopreventive effects have been attributed to compounds in which the Se moiety is methylated. These compounds are able to induce phase 2 enzymes which are involved in the cellular defense system that is regulated by the Nrf2 transcription factor. Selenoproteins best studied in cancer development are members of the glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) family. In various cancer cells and tissues, GPx2 and/or TrxR1 are up‐regulated. Interestingly, both enzymes are targets of Nrf2. An enhanced expression of these enzymes may represent a mechanism to counteract carcinogenic pathways. They may, however, also provide a selective advantage for pre‐existing tumor cells in guaranteeing survival and continuous proliferation.
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## Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable v
## Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable v