Selenium relieves oxidative stress, inflammation, and apoptosis within spleen of chicken exposed to mercuric chloride.

Mercuric chloride (HgCl) is a widely distributed environmental pollutant with multiorgan toxicity including immune organs such as spleen. Selenium (Se) is an essential trace element in animal nutrition and exerts biological activity to antagonize organ toxicity caused by heavy metals. The objective of this study was to explore the underlying mechanism of the protective effects of Se against spleen damage caused by HgCl in chicken. Ninety male Hyline brown chicken were randomly divided into 3 groups namely Cont, HgCl, and HgCl+Se group. Chicken were provided with the standard diet and nontreated water, standard diet and HgCl-treated water (250 ppm), and sodium selenite-treated diet (10 ppm) plus HgCl-treated water (250 ppm), respectively. After being fed for 7 wk, the spleen tissues were collected, and spleen index, the microstructure of the spleen, and the indicators of oxidative stress, inflammation, apoptosis as well as heat shock proteins (HSP) were detected. First, the results of spleen index and pathological examination confirmed that Se exerted an antagonistic effect on the spleen injury induced by HgCl. Second, Se ameliorated HgCl-induced oxidative stress by decreasing the level of malondialdehyde and increasing the levels of glutathione, glutathione peroxidase, and total antioxidant capacity. Third, Se attenuated HgCl-induced inflammation by decreasing the protein expression of nuclear factor kappa-B, inducible nitric oxide synthase, and cyclooxygenase-2, and the gene expression of interleukin (IL)-1β, IL-6, IL-8, IL-12β, IL-18 as well as tumor necrosis factor-α. Fourth, Se inhibited HgCl-induced apoptosis by downregulating the protein expression of BCL2 antagonist/killer 1 and upregulating the protein expression of B-cell lymphoma-2. Finally, Se reversed HgCl-triggered activation of HSP 60, 70, and 90. In conclusion, Se antagonized HgCl-induced spleen damage in chicken, partially through the regulation of oxidative stress, inflammatory, and apoptotic signaling.