Selenium regulates expression in rat liver of genes for proteins involved in iron metabolism

Suppression subtractive hybridization analysis in our laboratory recently r evealed that transferrin mRNA may be elevated in Se-deficient rat liver. In this work, we compared expression in rat liver of genes for transferrin, t ransferrin receptor, ferritin light and heavy chains, and iron-regulatory p roteins 1 and 2 in Se adequacy and deficiency. Weanling male Sprague-Dawley rats were fed Torula yeast diets supplemented with 0 or 0.15 mu g Se/kg di et as sodium selenite for 15 wk. Activity of cellular glutathione peroxidas e was virtually abolished in Se-deficient rat liver, whereas activity of gl utathione S-transferase was 43% higher than in Se-adequate liver. There wer e no differences in hematocrit, hemoglobin, or liver iron content. To exami ne differential gene expression, we used a multiplex relative reverse trans criptase-polymerase chain reaction method. Three of the six genes examined showed modest but consistent upregulation in Se deficiency. Transferrin mRN A was 30% more abundant in Se-deficient than in Se-adequate liver. For the transferrin receptor, the difference was 32%, and for iron regulatory prote in 1, it was 63%. No consistent differences were observed for iron regulato ry protein 2 or for ferritin light or heavy chain. These findings suggest a possible role for dietary Se in moderating iron metabolism.