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

Abstract

Mercuric chloride (HgCl2) 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 HgCl2 in chicken. Ninety male Hyline brown chicken were randomly divided into 3 groups namely Cont, HgCl2, and HgCl2+Se group. Chicken were provided with the standard diet and nontreated water, standard diet and HgCl2-treated water (250 ppm), and sodium selenite-treated diet (10 ppm) plus HgCl2-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 HgCl2. Second, Se ameliorated HgCl2-induced oxidative stress by decreasing the level of malondialdehyde and increasing the levels of glutathione, glutathione peroxidase, and total antioxidant capacity. Third, Se attenuated HgCl2-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 HgCl2-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 HgCl2-triggered activation of HSP 60, 70, and 90. In conclusion, Se antagonized HgCl2-induced spleen damage in chicken, partially through the regulation of oxidative stress, inflammatory, and apoptotic signaling.