Submitted to: Biological Trace Element Research
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/21/2008
Publication Date: 6/15/2008
Publication URL: http://handle.nal.usda.gov/10113/19368
Citation: Zeng, H., Botnen, J.H., Johnson, L.K. 2008. A selenium-deficient Caco-2 cell model for assessing differential incorporation of chemical or food selenium into glutathione peroxidase. Biological Trace Element Research. 123:98-108. Interpretive Summary: Selenium (Se) is an essential dietary component for mammals including humans, and there is increasing evidence for the efficacy of certain forms of selenium as cancer-chemopreventive compounds. In addition, selenium appears to have a protective effect at various stages of carcinogenesis including both the early and later stages of cancer progression. In the present study, we have developed the first Se-deficient Caco-2 cell culture model that has at least two potential applications related to Se bioavailability. First, the Se-deficient Caco-2 cells can be a useful tool to study cellular mechanisms related to Se bioavailability. Second, the Se-deficient Caco-2 cells can be used to assess the potential of Se supplements/food samples to induce GPx1 activity at cellular level. The information will be useful information for scientists and health-care professionals who are interested in Se and cancer prevention.
Technical Abstract: Assessing the ability of a selenium (Se) sample to restore cellular glutathione peroxidase (GPx1) activity in Se-deficient animals is the most commonly used method to determine Se bioavailability. Our goal is to establish a Se-deficient cell culture model with differential incorporation of Se chemical forms into GPx1, which may provide a new tool to study cellular mechanisms related to Se bioavailability. In the present study, we developed a Se-deficient Caco-2 cell model with a serum gradual reduction method. We then added various Se chemical forms with 15.6, 31.2, 62.5, or 125 nmol/L concentrations for 8, 24, 48, or 72 h. We found that selenite and se-(methyl)selenocysteine (SeMSC) had greater potential to restore GPx1 than selenomethionine (SeMet). Compared with 8, 24 or 48h, 72-h Se-treatment was a more sensitive time point to measure the potential of GPx1 restoration in all tested concentrations. In contrast to the GPx1 activity results, SeMet was better retained than selenite and SeMSC when provided at 62.5 nmol/L or higher concentrations. Based on restoration of GPx1 activity, the cellular bioavailability of Se from an extract of selenobroccoli after a simulated gastrointestinal digestion was comparable with that of SeMSC and SeMet. These findings are consistent with previous published data regarding selenite and SeMet bioavailability in animal models and Se chemical speciation studies with broccoli. Thus, Se-deficient Caco-2 cell model with differential incorporation of chemical or food forms of Se into GPx1 provides a useful model to study the cellular mechanisms of Se bioavailability.