Moksnes K, Norheim G
Acta Vet Scand. 1986;27(1):103-14. doi: 10.1186/BF03548563.
Fifty Norwegian-bred White Leghorn chickens, 20 weeks of age, were divided into 3 groups and fed a basal diet containing 0.09 mg Se/kg dry matter (D.M.). One group was given a supplement of 0.5 mg Se/kg as seleno-DL-methionine (Se-Met), another group 0.5 mg/kg as sodium selenite while one group served as control. After 10 weeks, all 3 groups were offered the basal diet without added selenium (Se) for a further 9 weeks. At the end of the supplementation period, significantly higher Se levels in blood and tissues were observed in the Se-Met group. These higher levels were not reflected in the glutathione peroxidase (GSH-Px) activity. During the first weeks of the depletion period, there was a steady decrease in Se levels and GSH-Px activity in blood and tissues in both the Se supplemented groups. However, Se levels in the group receiving sodium selenite fell almost to- those in the control group after 2 weeks, while the levels in the Se-Met group did not approach the control levels, even after 9 weeks. There were no differences as regards tissue GSH-Px activity between the 2 supplemented groups, which in both groups nearly reached the control level after 2 weeks. There was, however, a more rapid decrease in GSH-Px activity in whole blood in the sodium selenite group from week 0 to 5 as compared to the Se-Met group. The results obtained in this study support the theory that different forms of Se occupy separate metabolic pools in the body, and that the Se pool resulting from Se-Met supplementation can be mobilized for GSH-Px synthesis in a depletion period.