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

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• 作者：Shu Hao ; Junfa Hu ; Suquan Song ; Da Huang ; Haibing Xu ; Gang Qian ; Fang Gan ; Kehe Huang
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2016
• 出版时间：February 17, 2016
• 年：2016
• 卷：64
• 期：6
• 页码：1385-1393
• 全文大小：494K
• ISSN：1520-5118

文摘

Selenium (Se) is generally known as an essential micronutrient and antioxidant for humans and animals. Aflatoxin B<sub>1sub> (AFB<sub>1sub>) 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 AFB<sub>1sub>-induced immune toxicity. The aim of this present study is to investigate the protective effects of Se against AFB<sub>1sub> 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 AFB<sub>1sub>. The results showed that Se supplementation alleviated the immune toxicity of AFB<sub>1sub> 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 AFB<sub>1sub>. SeMet enhanced mRNA and protein expression of glutathione peroxidase 1 (GPx1), selenoprotein S (SelS), and thioredoxin reductase 1 without and with AFB<sub>1sub> treatments. Furthermore, knockdown of GPx1 and SelS by GPx1-specific siRNA and SelS-specific siRNA diminished the protective effects of SeMet against AFB<sub>1sub>-induced immune toxicity. It is concluded that SeMet diminishes AFB<sub>1sub>-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 AFB<sub>1sub>.