Abstract
Selenium (Se) is an essential and toxic trace mineral in animal diets. The current NRC turkey Se requirement is 0.2 µg Se/g diet for all life stages, higher than the published rat and mouse requirements. The studies that form the basis for the turkey requirement were performed over 50 years ago and based on prevention of Se-deficiency disease. With the genetic improvement of commercial turkey flocks and emerging new Se status biomarkers, we fed day-old male poults a Se-deficient (0.005 µg/g), vitamin E-adequate torula-based diet supplemented with graded levels of Se, from 0 to 5 µg/g, for 28 days. Poults supplemented with <0.05 µg/g had reduced growth, but there was no effect of high Se on growth. Se biomarkers responded hyperbolically to increasing dietary Se and reached plateaus at or before 0.4 µg/g. In deficiency, liver and kidney Se fell to <10% of Se-adequate levels. Activities of plasma GPX3; liver, kidney, pancreas and muscle GPX1; and liver, kidney, muscle and gizzard GPX4 all decreased to <10% in Se deficiency and reached plateau levels by 0.4 µg/g. In the same tissues, ≤6 out of 24 selenoprotein transcripts were downregulated to 2X Se-adequate levels in poults fed up to 5 µg/g diet. Liver Se increased to 5.6X Se-adequate levels with 5 µg/g diet. We conclude that the dietary Se level to maximize Se status biomarkers in growing turkey poults is 0.4 µg Se/g diet, double the current NRC requirement. Transcript expression is maximized at lower dietary Se levels than enzyme activities of the corresponding selenoproteins. Lastly, based on growth data, the turkey appears resistant to excess dietary Se, suggesting FDA Se supplementation limits can be safely raised. (Funded by USDA Hatch 1013496)
Detection of turkey coronavirus in commercial turkey poults in Brazil
