Differential protein expression due to Se deficiency and Se toxicity in rat liver.

Abstract There is a U-shaped dose-response between selenium (Se) status and health outcomes, but underlying metabolic processes are unclear. This study aims to identify candidate proteins in liver regulated by dietary Se, ranging from deficiency to toxic. Male rats (n=4) were fed graded Se concentrations as selenite for 28 days. Bulk Se analysis was performed by ICP-MS on both soluble and insoluble fractions. Soluble fraction samples were chromatographically separated for identification of selenocompounds by SEC-ICP-MS and protein quantification by LC-MS/MS. Bioinformatics analysis compared low-Se (0 and 0.08 µg Se g−1) and high-Se (0.8, 2 and 5 µg Se g−1) with adequate-Se (0.24 µg Se g−1) diets. Major breakpoints for Se were seen at 0.8 and 2 µg Se g−1 in the insoluble and soluble fractions, respectively. Glutathione peroxidase 1 protein abundance reached a plateau at ≥0.08 µg Se g−1diet; Se bound to selenium binding protein 2 was observed with 2 and 5 µg Se g−1 Se. The extreme diets presented the highest number of differentially expressed (P value