Selenium Alleviates Aflatoxin B1-Induced Immune Toxicity through Improving Glutathione Peroxidase 1 and Selenoprotein S Expression in Primary Porcine Splenocytes.

Selenium (Se) is generally known as an essential micronutrient and antioxidant for humans and animals. Aflatoxin B1 (AFB1) is a frequent contaminant of food and feed, causing immune toxicity and hepatotoxicity. Little has been done about the mechanisms of how Se protects against AFB1-induced immune toxicity. The aim of this present study is to investigate the protective effects of Se against AFB1 and the underlying mechanisms. The primary splenocytes isolated from healthy pigs were stimulated by anti-pig-CD3 monoclonal antibodies and treated by various concentrations of different Se forms and AFB1. The results showed that Se supplementation alleviated the immune toxicity of AFB1 in a dose-dependent manner, as demonstrated by increasing T-cell proliferation and interleukin-2 production. Addition of buthionine sulfoximine abrogated the protective effects of SeMet against AFB1. SeMet enhanced mRNA and protein expression of glutathione peroxidase 1 (GPx1), selenoprotein S (SelS), and thioredoxin reductase 1 without and with AFB1 treatments. Furthermore, knockdown of GPx1 and SelS by GPx1-specific siRNA and SelS-specific siRNA diminished the protective effects of SeMet against AFB1-induced immune toxicity. It is concluded that SeMet diminishes AFB1-induced immune toxicity through increasing antioxidant ability and improving GPx1 and SelS expression in splenocytes. This study suggests that organic selenium may become a promising supplementation to protect humans and animals against the decline in immunity caused by AFB1.

Syntheses, structures and photophysical properties of heterotrinuclear Zn2Ln clusters (Ln = Nd, Eu, Tb, Er, Yb).

Heterotrinuclear Zn(2)Ln (Ln = Nd 2, Eu 3, Tb 4, Er 5, Yb 6) clusters [(Znq(2))(2)](mu-CH(3)COO){Ln(hfac)(2)} (q = 8-hydroxylquinolinate, hfac = hexafluoroacetylacetonate) have been synthesized. The Zn(2)Ln framework is ligated by two q ligands featuring mu-phenoxo and two q ligands featuring mu(3)-phenoxo coordination modes, and one mu-CH(3)COO(-) anions. Since the short intramolecular separations of Zn...Ln (ca. 3.354-3.373 A) allow energy transfer from Znq(2)-based sensitizers to the Ln(III) centres through two energy transfer pathways, the lanthanide luminescence is indeed "lighted up" by excitation of the Znq(2)-based chromopores. Photophysical measurements revealed that these Zn(2)Ln complexes exhibit the so-called "dual emission" originating from both Znq(2)-based luminophores and lanthanide emitters. By virtue of the dual luminescence with complementary colours, the Znq(2)-based cyan emission and Eu(III)-centred red luminescence are combined to generate a white-light emission in the Zn(2)Eu (3) complex.