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Abstract
Deoxynivalenol (DON) is a common contaminant of grain worldwide and is often detected in the human diet and animal feed. Selenium is an essential trace element in animals. It has many biological functions. The role of selenium in the body is mainly orchestrated by selenoprotein. Glutathione peroxidase (GPx) also exists widely in the body and has attracted much attention due to its high antioxidant capacity. In order to explore the effect of the GPx1 gene on toxicity of DON, in this study, we overexpressed or knockdown GPx1 in porcine splenic lymphocytes, then added different concentrations of DON (0.1025, 0.205, 0.41, and 0.82 μg/mL) and sodium selenite (2 μmol/L) to the culture system. Using various techniques, we detected antioxidant function, free radical content, cell apoptosis, and methylation-related gene expression to explore the effect of GPx1 expression on DON-induced cell damage. We also explored whether selenium can antagonize the toxicity of DON in these two cell models and revealed the protective effect of sodium selenite on DON-induced cell damage in GPx1-overexpressing or knockdown splenic lymphocytes. Finally, our findings revealed the following: (1) GPx1 can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes. (2) Na2SeO3 (2 μmol/L) can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes, and this effect is more significant in GPx1-overexpressing cells than in GPx1-knockdown cells. (3) DON can cause oxidative damage, apoptosis, and methylation injury in GPx1-overexpressing or knockdown pig splenic lymphocytes in a concentration-dependent manner. (4) Na2SeO3 (2 μmol/L) can antagonize the toxic effect of DON on GPx1-overexpressing or knockdown pig splenic lymphocytes. Our findings may have important implications for food/feed safety, human health, and environmental protection.
Highlights
Mycotoxin is a secondary metabolite of mold
(2) Na2SeO3 (2 μmol/L) can regulate the antioxidant capacity, apoptosis rate, and expression of DNA methylation-related genes in pig splenic lymphocytes, and this effect is more significant in GPx1-overexpressing cells than in GPx1-knockdown cells
A study found that the oxidative damage caused by Fusarium toxins is likely to be due to destruction of the body’s antioxidant system and acceleration of the production of free radicals [8], which has been confirmed in Caco-2 and HepG2 cells [9]
Summary
Mycotoxin is a secondary metabolite of mold. It can exist in grain during various stages of harvesting and food processing and is generally stable and not destroyed or removed. A study found that the oxidative damage caused by Fusarium toxins is likely to be due to destruction of the body’s antioxidant system and acceleration of the production of free radicals [8], which has been confirmed in Caco-2 and HepG2 cells [9]. When DON acts on spleen lymphocytes, it can cause oxidative damage to cells, affect the expression of immunoglobulins, and change the antioxidant index. In a study of the changes in the antioxidant index of spleen lymphocytes induced by DON, Ren and colleagues [18] used DON at different doses (0.006, 0.3, 1.5, and 7.5 μg/mL) to direct the pig spleen lymphocytes and found that the SOD, catalase (CAT), glutathione peroxidase (GPx), and GSH content decreased significantly compared with the control group, whereas the malondialdehyde (MDA) content increased significantly. We observe whether there is any change in the antagonism of selenium to DON when GPx1 is too much or too little
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