Effect of selenium supplementation on the distribution of selenium among plasma proteins of a patient with maple syrup urine disease.

Selenium (Se) status was studied in a patient with classical maple syrup urine disease (MSUD) receiving Se supplement. The basal plasma Se concentration was 0.06 mumol/l increasing to 2.1 mumol/l after 40 days of supplementation. When the plasma Se distribution was analysed by gel filtration, a major peak was seen close to the high molecular weight proteins with a second peak in the albumin region. When the Se dose was decreased in a stepwise manner from 50 micrograms/day to 25 micrograms/day and then to 17 micrograms/day plasma Se decreased, but the proportion of plasma Se in the two protein peaks did not change. In a healthy girl not supplemented with Se, the proportion of plasma Se in the albumin region was somewhat lower. In the MSUD patient glutathione peroxidase activity was initially low, and increased ten-fold during Se supplementation. The study indicates that the Se requirement for plasma glutathione peroxidase activity was fulfilled at the lowest dose of Se used and that Se is incorporated into several plasma proteins after supplementation.

Distribution of selenium and glutathione peroxidase in plasma compared in healthy subjects and rheumatoid arthritis patients.

The distribution of selenium and glutathione peroxidase activity in plasma was compared in samples from healthy adult controls and patients with rheumatoid arthritis. Plasma was separated by gel filtration, and selenium was measured in the eluted fractions by means of graphite furnace atomic absorption spectrometry with Zeeman background correction. Most of the selenium in plasma of healthy controls was seen in proteins that migrated close to immunoglobulin G, and that had an apparent molecular weight at the peak of 174 kDa. One major peak of glutathione peroxidase activity with an apparent molecular weight of 99 kDa was unmatched by any significant peak in selenium content. Thus, there was only limited correspondence between the elution patterns of selenium and glutathione peroxidase activity. Also, in patients with active rheumatoid arthritis, selenium was distributed amongst plasma proteins with a wide range of molecular weights. The major selenium peak was less pronounced in patients, but the amount of selenium in other parts of the chromatogram was not different from that in controls. Further work is necessary to define the occurrence of different selenoproteins in plasma in patients and in healthy subjects.

Effect of selenium supplementation on the distribution of selenium in plasma proteins of healthy subjects.

The influence of an increased intake of selenium on the distribution of this element among plasma proteins was studied. 200 micrograms of yeast selenium was given to healthy subjects daily for 8 weeks, and then the subjects refrained from selenium supplementation for 16 weeks. Plasma selenium increased almost two-fold during supplementation, and most of the increase occurred during the first 4-week-period. Plasma glutathione peroxidase activity increased only marginally. At all times studied, most of the selenium in plasma was located in proteins, migrating close to immunoglobulin G on gel filtration. The selenium content of this fraction was only moderately increased after supplementation for 8 weeks, and instead more marked increases occurred in the regions for high-molecular-weight proteins and albumin. This change implied that the distribution of selenium approached that of total protein, and we therefore conclude that most of the increase in plasma selenium occurred via unspecific incorporation of selenium into a wide variety of proteins. Sixteen weeks after the end of supplementation the selenium distribution had essentially returned to that before supplementation.