Previous study indicated that inclusion of an algae-based antioxidant as an antioxidative agent [EconomasE, Alltech, Nicholasville, KY; EcoE] significantly reduced the amount of vitamin E (VE) required in broiler diets without compromising performance and meat quality. To assess the mechanisms related to the VE-saving activity of EcoE, as well as other potential functions related to EcoE and VE supplementation, we analyzed gene expression profiles of breast muscle from broilers fed a control diet, the control diet + 50 IU of VE/kg, the control diet + 100 IU of VE/kg, or the control diet + 200 g of EcoE/ton. Evaluation of the serum antioxidant capacity indicated that dietary supplementation of either a high level of VE (50 or 100 IU of VE/kg) or EcoE significantly improved bird antioxidant status. Analysis of gene expression profiles indicated that expression of 542 genes of the breast muscle were altered (P < 0.05, fold change >1.2) by dietary treatments, of which a significant part were commonly regulated by EcoE and VE (especially the control diet + 50 IU of VE/kg). In addition to the process of cellular oxidation, gene ontology analysis indicated the involvement of EcoE and VE on cell morphology, skeletal and muscular system development and function, immune response, and multiple metabolic processes, including lipid, carbohydrate, and drug metabolism. Results of this experiment indicate that the biological roles of high VE, including its activity as an antioxidant, can be greatly mimicked at the transcriptional level by EcoE, and they suggest a relationship of functional redundancy between VE and EcoE in the broiler diets.

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Selenium is a trace element that, although toxic in higher concentrations, is essential for human and animal health. In this study, we looked at microarray-based gene expression patterns from liver and gastrocnemius tissues in mice fed either a selenium-deficient diet or diets containing sodium selenite, selenomethionine, or a yeast-derived selenium supplement. A p value cutoff of 0.01 was used to identify a select set of selenium-responsive genes that were consistently differentially expressed across three age groups of mice with both ANOVA and t test analyses. A total of 19 gene transcripts were found to be differentially expressed across the three age groups with at least one selenium-deficient/selenium-supplemented diet comparison. Of those 19 genes, 12 had been previously identified as selenoprotein-encoding genes, and four of the genes, Gpx1, Selh, Sep15, and Sepw1, were differentially expressed in both tissues, all three mouse age groups, and all three diet comparisons. Activities associated with non-selenoproteins encoded by selenium-responsive genes included transport and stress response. The selenophosphate synthetase 2 gene Sephs2 in gastrocnemius tissue and the solute carrier gene Slc48a1 in liver tissue, both up-regulated with selenium-deficient diets compared to all three selenium-supplemented diets, are previously overlooked candidates for dietary selenium marker genes.

During a study of spinal cord injury (SCI), mice in our colony were treated with the anthelmintic fenbendazole to treat pinworms detected in other mice not involved in the study. As this was not part of the original experimental design, we subsequently compared pathological and functional outcomes of SCI in female C57BL/6 mice who received fenbendazole (150 ppm, 8 mg/kg body weight/day) for four weeks prior to moderate contusive SCI (50 kdyn force) as compared to mice on the same diet without added fenbendazole. The fenbendazole-treated mice exhibited improved locomotor function, determined using the Basso mouse scale, as well as improved tissue sparing following contusive SCI. Fenbendazole may exert protective effects through multiple possible mechanisms, one of which is inhibition of the proliferation of B lymphocytes, thereby reducing antibody responses. Autoantibodies produced following SCI contribute to the axon damage and locomotor deficits. Fenbendazole pretreatment reduced the injury-induced CD45R-positive B cell signal intensity and IgG immunoreactivity at the lesion epicenter six weeks after contusive SCI in mice, consistent with a possible effect on the immune response to the injury. Fenbendazole and related benzimadole antihelmintics are FDA approved, exhibit minimal toxicity, and represent a novel group of potential therapeutics targeting secondary mechanisms following SCI.