2-Hydroxy-(4-methylseleno)butanoic acid is used by intestinal Caco-2 Cells as a source of selenium and protects against oxidative stress

Abstract

<p>Background: Selenium (Se) participates in different functions in humans and other animals through its incorporation</p><p>into selenoproteins as selenocysteine. Inadequate dietary Se is considered a risk factor for several chronic diseases</p><p>associated with oxidative stress.</p><p>Objective: The role of 2-hydroxy-(4-methylseleno)butanoic acid (HMSeBA), an organic form of Se used in animal</p><p>nutrition, in supporting selenoprotein synthesis and protecting against oxidative stress was investigated in an in vitro</p><p>model of intestinal Caco-2 cells.</p><p>Methods: Glutathione peroxidase (GPX) and thioredoxin reductase (TXNRD) activities, selenoprotein P1 protein</p><p>(SELENOP) and gene (SELENOP) expression, and GPX1 and GPX2 gene expression were studied in Se-deprived (FBS</p><p>removal) and further HMSeBA-supplemented (0.1–625 μM, 72 h) cultures. The effect of HMSeBA supplementation (12.5</p><p>and 625 μM, 24 h) on oxidative stress induced by H2O2 (1 mM) was evaluated by the production of reactive oxygen</p><p>species (ROS), 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyl residues compared with a sodium selenite</p><p>control (SS, 5 μM).</p><p>Results: Se deprivation induced a reduction (P < 0.05) in GPX activity (62%), GPX1 expression, and both SELENOP</p><p>(33%) and SELENOP expression. In contrast, an increase (P < 0.05) in GPX2 expression and no effect in TXNRD activity</p><p>(P = 0.09) were observed. HMSeBA supplementation increased (P < 0.05) GPX activity (12.5–625 μM, 1.68–1.82-fold)</p><p>and SELENOP protein expression (250 and 625 μM, 1.87- and 2.04-fold). Moreover, HMSeBA supplementation increased</p><p>(P < 0.05) GPX1 (12.5 and 625 μM), GPX2 (625 μM), and SELENOP (12.5 and 625 μM) expression. HMSeBA (625 μM)</p><p>was capable of decreasing (P < 0.05) ROS (32%), 4-HNE adduct (49%), and protein carbonyl residue (75%) production</p><p>after H2O2 treatment.</p><p>Conclusion: Caco-2 cells can use HMSeBA as an Se source for selenoprotein synthesis, resulting in protection against</p><p>oxidative stress. J Nutr 2019;149:2191–2198.</p>