Selenium-Enriched Yeast Relieves Hexavalent Chromium Toxicity by Inhibiting NF-κB Signaling Pathway in Broiler...

This study was conducted to investigate the molecular mechanisms of selenium (Se) antagonism of hexavalent chromium (Cr⁶⁺)-induced toxicity. Potassium dichromate (K₂Cr₂O₇) and selenium-enriched yeast (SeY) were used to construct the single Cr⁶⁺ and combined Se/Cr⁶⁺ exposure broiler models, and then the broilers were randomly divided into four groups (C group, Se group, Se/Cr⁶⁺ group, and Cr⁶⁺ group). After a 42-day experiment, the spleen tissues of broilers were excised and weighted. The antagonistic mechanisms of Se and Cr⁶⁺ were evaluated using histopathological assessment, serum biochemical tests, oxidative stress kits, ELISA, qPCR, and Western blotting. On the whole, there were no significant changes between the C and Se groups. The spleen organ index in the Cr⁶⁺ group was significantly decreased, but SeY increased spleen organ index to a certain extent. The levels of SOD and GSH were reduced, and the MDA content was elevated by Cr⁶⁺; however, these changes were mitigated by Se/Cr⁶⁺ exposure. Importantly, Cr⁶⁺ exposure induced a series of histopathological injuries in broiler spleen tissues, while these symptoms were significantly relieved in the Se/Cr⁶⁺group. Furthermore, Cr⁶⁺ significantly decreased the levels of T-globulin, IgA, IgM, and IgG in serum. Contrarily, dramatically more T-globulin IgA, IgM, and IgG were found in the Se/Cr⁶⁺group than in the Cr⁶⁺ group. Revealed by the results of qPCR and WB, the expressions of NF-κB, IκBα, and p-IκBα were upregulated in Cr⁶⁺ groups, while they were downregulated in Se/Cr⁶⁺ group compared to that in Cr⁶⁺ group. Besides IFN-γ and IL-2, the expressions of pro-inflammatory cytokines were significantly increased by Cr⁶⁺ exposure, but the SeY supplement relived the expression levels mediated by Cr⁶⁺ exposure. In conclusion, our findings suggest SeY has biological activity that can protect broiler spleens from immunosuppression and inflammation induced by Cr⁶⁺, and we speculate that the NF-κB signaling pathway is one of its mechanisms.