Kehe Huang
Nanjing Agricultural University, China
Title: SeMet protects against AFB1 and OTA - induced toxicity by improving selenoprotein expressions
Biography
Biography: Kehe Huang
Abstract
In recent years, numerous studies indicated that organic Se is more bioavailable. However, little has been done about the mechanisms of how selenomethionine (SeMet) protects against AFB1 and OTA - induced toxicity. Firstly, the primary splenocytes isolated from healthy pigs were stimulated by anti-pig-CD3 monoclonal antibodies and treated by various concentrations of SeMet and AFB1. The results showed that SeMet supplementation alleviated the immunotoxicity of AFB1 in a dose-dependent manner. 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 immunotoxicity. Secondly, the protective effects of SeMet against OTA-induced nephrotoxicity were investigated in PK15 cells. The results showed that OTA induced nephrotoxicity in a dose-dependent manner. SeMet at 0.5, 1, 2 and 4 µM had significant protective effects against OTA-induced nephrotoxicity. Furthermore, SeMet enhanced the activity, mRNA and protein expression of GPx1, mRNA expression of GPx4, mRNA expression of thioredoxin reductase 1 in the presence and absence of OTA. Knock-down of GPx1 by using a GPx1-specific siRNA eliminated the protective effects of SeMet against OTA-induced nephrotoxicity. In conclusion, SeMet diminishes AFB1-induced immunotoxicity and OTA-induced nephrotoxicity by improving selenoprotein expression in PK15 cells.