Selenium repletion is the re-establishment of correct selenium status. It is known that the Western diet is typically deficient in selenium. As a result many of the individuals within such populations are deficient in the mineral. Clark’s seminal study on the effects of selenium supplements in 1996 (here) showed that 200 μg of selenium was able to lower the mortality and morbidity of cancer by 50 %. The effects of selenium in Clark’s study highlighted the level of deficiencies within the study subjects and the detrimental effects of poor selenium status. Selenium deficiency may lead to cancer formation because selenium is required for the glutathione peroxidase enzyme which is necessary to allows reduced glutathione to act as a cellular antioxidant by facilitating the conversion of hydrogen peroxide to water (figure 1). A deficiency of the mineral causes an increase in cellular free radical damage, and this can initiate the disease process. Studies investigating selenium repletion are therefore of interest nutritionally.
The kinetics of selenium repletion are complex, but a number of studies have shown that dietary selenium can quickly cause elevations in plasma levels of glutathione peroxidase when supplements are taken. For example, in one study1, researchers investigated the effects of 240 μg per day of intravenous sodium selenite on the selenium repletion of three children. The children were chosen for the study because they had gastrointestinal malabsorption that meant that they were not correctly absorbing selenium. As a result they had very poor selenium status and were considered deficient in the mineral. The plasma glutathione peroxidase activity of the subjects was between 4 and 24 % of normal and the erythrocyte levels of glutathione peroxidase was between 4 and 14 % of normal. Plasma glutathione peroxidase returned to normal range following 4 to 5 weeks of the intravenous infusion. However, during this time the red blood cell glutathione peroxidase activity remained essentially unchanged.
Selenium repletion of red blood cell glutathione peroxidase activity took 3 to 4 months to occur in the subjects. This suggests that plasma glutathione activity increases initially with supplementation, but red blood cell glutathione peroxidase activity requires a much longer period of selenium repletion. This likely reflects the time taken for new erythrocytes to be synthesised in the presence of elevated plasma selenium concentrations. Therefore selenium repletion is a multiphase event and increased selenium intake is required for many months before selenium repletion is complete. Similar findings have been reported following selenium repletion using intravenous infusions elsewhere (here). Although these subjects underwent intravenous administration of the selenium due to their gastrointestinal malabsorption, oral selenium is able to raise plasma levels and cause selenium repletion. Long-term supplementation is however necessary before the full benefits of selenium repletion are seen.