Effects of excessive selenium supplementation to diet contaminated with deoxynivalenol on blood phagocytic activity and antioxidative status of broilers

Abstract

This study examined the effects of excessive dietary supplementation with organic selenium on phagocytic activity and antioxidative status of chickens for fattening fed diet contaminated with deoxynivalenol (DON). Sixty chickens of Ross 308 hybrids were at day of hatching divided into four groups with 15 birds in each. The background DON dietary levels in both negative and positive control groups were 0.2 mg/kg. The complete feed for positive control group was supplemented with Se dose 1 mg/kg in the form of Se-yeast. Group 3 was fed diet with DON level 3 mg/kg while diet for group 4 combined DON level 3 mg/kg with a excessive supplement of Se-yeast (Se dose 1 mg/kg). After 6 weeks of dietary intake, six randomly-chosen chickens from each group were sampled. Feeding of contaminated diet resulted in significantly reduced blood phagocytic activity (19.5 ± 1.1% in the negative control vs. 12.8 ± 0.8% in the DON-treated group, p < 0.05). Se-yeast supplemented to the DON contaminated diet prevented suppression of phagocytic activity. Dietary intake of DON at levels 3 mg/kg did not influence the plasma α-tocopherol level while excessive dietary Se dose reduced it in both Se supplemented groups. Neither the birds of DON-treated group nor the birds from group 4 with DON and Se-yeast showed any response in plasma γ-glutamyltransferase (GGT) activity. Subtoxic dietary level of DON significantly increased the activity of glutathione peroxidase (GPx) in the duodenal mucosa, while additional Se supplementation prevented such a response to mycotoxin. On the other hand, both Se supplemented groups showed significantly elevated GPx activities in blood, liver and kidney, (p < 0.05). The results suggest a potential ability of excessive supplementation of organic selenium to prevent the blood phagocytic activity suppression and changes in GPx activity in duodenal tissue induced in broilers by subtoxic dietary levels of DON.