RESUMO
Cadmium (Cd) exposure can cause multiple organ damage in humans and animals by causing oxidative stress. Organic selenium can antagonize the toxic damage of heavy metals by exerting antioxidant effects. Oxidative stress can activate NLRP3/Caspase1-dependent pyroptosis, but it is not clear whether yeast selenium (Se Y) can antagonize Cd-induced pyroptosis in the chicken liver. In this experiment, we studied the effects of CdCl2 single, Se Y single, and combined exposure on the pyroptosis of chicken liver. The results showed that Cd exposure induced oxidative stress in the chicken liver, and the expression of Sepx1, SelU, SelT, GPx1, GPx4, Dio1, Dio2, Dio3, TrxR1, TrxR2, TrxR3, SelH, SelI, SelO, SelK, SelPb, Selpp, and Sel15 decreased. In addition, NLRP3 inflammasome complex (NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing (ASC), and pro-Caspase1), Cysteinyl aspartate specific proteinase (Caspase1), Interleukin-ß (IL-1ß), and Interleukin-18 (IL-18) were upregulated. The combined treatment of Se Y and Cd found that the antioxidant level and the expression level of selenoprotein recovered to the Se group, and the liver pyroptosis decreased. Principal component analysis and correlation analysis screened out that selenoprotein O (SelO) is negatively correlated with pyroptosis-related genes. In short, our data shows that Se Y exerts an antioxidant effect by increasing the expression of selenoproteins and antagonizing the pyroptosis of chicken liver induced by Cd. This study provides new ideas for the field of heavy metal toxicology research. And the selected SelO has an important reference significance for follow-up research.