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

SIMPLE SUMMARY: Hexavalent chromium is a common environmental pollution. It has been reported that hexavalent chromium threatens the health of humans and animals, so it is necessary to develop new, effective mitigation methods. Selenium is an indispensable micronutrient recently shown to be able to...

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Detalles Bibliográficos
Autores principales: Zhao, Yanbing, Hao, Dezheng, Zhang, Huan, Wang, Jingqiu, Liu, Ci
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8772575/
https://www.ncbi.nlm.nih.gov/pubmed/35049769
http://dx.doi.org/10.3390/ani12020146
Descripción
Sumario:SIMPLE SUMMARY: Hexavalent chromium is a common environmental pollution. It has been reported that hexavalent chromium threatens the health of humans and animals, so it is necessary to develop new, effective mitigation methods. Selenium is an indispensable micronutrient recently shown to be able to resist the toxicity of heavy metals. Selenium-enriched yeast has a high content of total selenium, which has the advantages of a high absorption rate and safety. Potassium dichromate and selenium-enriched yeast were used to construct single hexavalent chromium and combined selenium/hexavalent-chromium-exposed broiler models. Additionally, the ability to relieve the hexavalent chromium toxicity of selenium along with the molecular mechanisms focusing on inflammation induced by the NF-κB signaling pathway was investigated in this study. Histopathological assessment, serum biochemical tests, oxidative stress kits, enzyme-linked immunosorbent assay, quantitative real-time PCR, and Western blotting were used to detect indicators. We found that the oxidative stress induced by hexavalent chromium triggers NF-κB pathway-driven inflammatory responses in the broiler spleen and further reduces the immune function of broilers. Selenium-enriched yeast protects the spleen from the toxicity of hexavalent chromium exposure through inhibiting the NF-κB signaling pathway. ABSTRACT: This study was conducted to investigate the molecular mechanisms of selenium (Se) antagonism of hexavalent chromium (Cr(6+))-induced toxicity. Potassium dichromate (K(2)Cr(2)O(7)) and selenium-enriched yeast (SeY) were used to construct the single Cr(6+) and combined Se/Cr(6+) exposure broiler models, and then the broilers were randomly divided into four groups (C group, Se group, Se/Cr(6+) group, and Cr(6+ )group). After a 42-day experiment, the spleen tissues of broilers were excised and weighted. The antagonistic mechanisms of Se and Cr(6+) 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 Cr(6+) 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 Cr(6+); however, these changes were mitigated by Se/Cr(6+) exposure. Importantly, Cr(6+) exposure induced a series of histopathological injuries in broiler spleen tissues, while these symptoms were significantly relieved in the Se/Cr(6+)group. Furthermore, Cr(6+) 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/Cr(6+)group than in the Cr(6+) group. Revealed by the results of qPCR and WB, the expressions of NF-κB, IκBα, and p-IκBα were upregulated in Cr(6+) groups, while they were downregulated in Se/Cr(6+) group compared to that in Cr(6+) group. Besides IFN-γ and IL-2, the expressions of pro-inflammatory cytokines were significantly increased by Cr(6+) exposure, but the SeY supplement relived the expression levels mediated by Cr(6+) exposure. In conclusion, our findings suggest SeY has biological activity that can protect broiler spleens from immunosuppression and inflammation induced by Cr(6+), and we speculate that the NF-κB signaling pathway is one of its mechanisms.